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Macrophage plasticity: signaling pathways, tissue repair, and regeneration
Lingfeng Yan, Jue Wang, Xin Cai and 6 more
MedComm · 2024 · Review · CC BY
Abstract
Macrophages are versatile immune cells with remarkable plasticity, enabling them to adapt to diverse tissue microenvironments and perform various functions. Traditionally categorized into classically activated (M1) and alternatively activated (M2) phenotypes, recent advances have revealed a spectrum of macrophage activation states that extend beyond this dichotomy. The complex interplay of signaling pathways, transcriptional regulators, and epigenetic modifications orchestrates macrophage polarization, allowing them to respond to various stimuli dynamically. Here, we provide a comprehensive overview of the signaling cascades governing macrophage plasticity, focusing on the roles of Toll‐like receptors, signal transducer and activator of transcription proteins, nuclear receptors, and microRNAs. We also discuss the emerging concepts of macrophage metabolic reprogramming and trained immunity, contributing to their functional adaptability. Macrophage plasticity plays a pivotal role in tissue repair and regeneration, with macrophages coordinating inflammation, angiogenesis, and matrix remodeling to restore tissue homeostasis. By harnessing the potential of macrophage plasticity, novel therapeutic strategies targeting macrophage polarization could be developed for various diseases, including chronic wounds, fibrotic disorders, and inflammatory conditions. Ultimately, a deeper understanding of the molecular mechanisms underpinning macrophage plasticity will pave the way for innovative regenerative medicine and tissue engineering approaches.
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From PubMed Central, U.S. National Library of Medicine, as current on Oct 20, 2026. Paragraph numbers are ours, so an answer can point at one.
INTRODUCTION
Macrophages, the versatile sentinels of the innate immune system, play critical roles in host defense, tissue homeostasis, and disease pathogenesis. Macrophages exhibit extraordinary plasticity, enabling them to adapt to diverse tissue microenvironments and perform various functions. This plasticity is exemplified by the ability of macrophages to polarize into distinct functional states in response to various stimuli, a process orchestrated by complex signaling pathways and transcriptional networks. In the past decade, there has been a surge of interest in elucidating the molecular mechanisms governing macrophage plasticity and their implications for tissue repair and regeneration. Macrophages play pivotal roles in all stages of the tissue repair process, from the initial inflammatory response to the resolution of inflammation and tissue remodeling.,, Dysregulation of macrophage function can lead to impaired wound healing, fibrosis, and chronic inflammation, underscoring the importance of understanding the signaling pathways that control macrophage activation states. Recent studies have shed light on the complex network of transcription factors, epigenetic regulators, and metabolic pathways that shape the macrophage transcriptional landscape and functional properties.,,,,
At present, the classification of macrophages into M1 and M2 types has been widely adopted in scientific research.,,,,,,, Through this extreme classification, macrophages are divided according to the functional differences of proinflammatory bactericidal and anti‐inflammatory and anti‐inflammatory prorepair.,, While this dichotomy provided a valuable framework for understanding macrophage heterogeneity, recent advances in single‐cell technologies and systems biology approaches have revealed a spectrum of activation states that extend beyond the M1/M2 paradigm., Therefore, further research is necessary to reconcile these findings and provide a more comprehensive understanding of macrophage phenotypes and functions. Despite this ongoing debate, the M1 and M2 classification continues to describe the different polarization states of macrophages in the study of tissue healing. During tissue repair, M1 and M2 macrophages fulfill distinct functions, and the timely transition of macrophages from an M1 to an M2 phenotype plays a critical role in wound healing and tissue regeneration.
Through this review, we aim to clarify the key pathways and epigenetic regulation that regulate the polarization of macrophages and discuss their roles in the repair and regeneration of various tissue damage to provide ideas and approaches for clinically diagnosing and treating macrophages as targets. The review is structured into four main sections. In the first section, we provide an overview of the historical perspective on macrophage plasticity and the evolution of the M1/M2 paradigm. We then delve into the spectrum of macrophage activation states revealed by recent single‐cell studies and discuss the limitations of the traditional classification system. The second section focuses on the signaling pathways that control macrophage polarization, emphasizing the roles of TLRs, signal transducer and activator of transcription (STAT) proteins, nuclear receptors, and microRNAs (miRNAs). We also discuss the emerging concepts of macrophage metabolic reprogramming and epigenetic regulation, highlighting their importance in shaping macrophage functional properties. The third section explores the functional significance of macrophage plasticity in tissue repair and regeneration, providing examples from cutaneous wound healing, skeletal muscle regeneration, and liver repair. We discuss macrophages’ dynamic roles in the repair process's different stages and the consequences of macrophage dysfunction in pathological conditions. The final section addresses the therapeutic potential of targeting macrophage polarization pathways, discussing the current strategies and future directions for modulating macrophage function in chronic wounds, fibrotic diseases, and inflammatory disorders.
MACROPHAGE PLASTICITY: FROM HISTORICAL ORIGINS TO CONTEMPORARY INSIGHTS
Macrophages, the versatile sentinels of the immune system, exhibit remarkable plasticity that enables them to adapt to diverse tissue microenvironments and perform a wide array of functions. First discovered by Élie Metchnikoff in 1882, these phagocytic cells were recognized for their roles in immunity and inflammation., Over the past century, our understanding of macrophage heterogeneity and plasticity has dramatically expanded, revealing their critical involvement in tissue homeostasis, wound healing, and disease pathogenesis. The traditional M1/M2 classification system, proposed by Mills et al. in 2000, provided a valuable framework for understanding macrophage polarization. M1 macrophages, activated by interferon‐γ (IFN‐γ) and lipopolysaccharide (LPS), exhibit proinflammatory properties and potent microbicidal activity. In contrast, M2 macrophages, induced by interleukin‐4 (IL‐4) and IL‐13, display anti‐inflammatory and tissue‐repair functions. While this dichotomy captures the extremes of macrophage activation, recent advances have revealed a spectrum of activation states that extend beyond the M1/M2 paradigm. This section discusses the historical origins of macrophage plasticity research and highlights the latest discoveries that have reshaped our understanding of this phenomenon. We explore the molecular mechanisms underlying macrophage plasticity, including transcriptional regulation, epigenetic modifications, and metabolic reprogramming. Furthermore, we discuss the functional significance of macrophage plasticity in health and disease, focusing on tissue‐specific adaptations and the role of trained immunity. Finally, we outline this rapidly evolving field's challenges and future directions.
Historical perspective on macrophage plasticity
Macrophage plasticity emerged in the 1960s when Mackaness et al.,,,,, reported two distinct macrophage activation states responding to cytokines. Type 1 macrophages, now known as M1, exhibited enhanced microbicidal activity against intracellular pathogens like Mycobacterium tuberculosis. Type 2 macrophages, now called M2, dampened inflammation and promoted extracellular matrix remodeling. In the 1980 and 1990s, the phenotypic and functional differences between M1 and M2 macrophages came into sharper focus. Stein et al. found that M1 macrophages produced high levels of proinflammatory cytokines, such as tumor necrosis factor‐α (TNF‐α), IL‐1, IL‐6, and IL‐12. This enabled them to stimulate T‐cell responses and potently unleash oxidative attacks against pathogens. Conversely, M2 macrophages secreted anti‐inflammatory cytokines like IL‐10 and expressed high arginase‐1 (ARG‐1) levels, allowing them to suppress immune responses and promote tissue repair. Based on arginine metabolism, the M1/M2 classification system was consolidated by Mills et al. in 2000, drawing parallels with T helper 1 (Th1) and Th2 lymphocyte polarization. While this dichotomy provided a helpful framework, it oversimplified the complex spectrum of macrophage activation states observed in vivo (Table 1).
M1 macrophages
M1 macrophages, also referred to as classically activated or proinflammatory macrophages, are induced by exposure to bacterial products like LPS and inflammatory cytokines such as IFN‐γ and TNF‐α., This activation state is characterized by the expression of specific surface markers, including CD80, CD86, and major histocompatibility complex (MHC) class II molecules, and the production of proinflammatory cytokines and mediators., Key markers and functions of M1 macrophages include (a) Cytokine production: M1 macrophages secrete high levels of proinflammatory cytokines such as TNF‐α, IL‐1 beta (IL‐1β), IL‐6, IL‐12, and IL‐23. These cytokines orchestrate the inflammatory response, recruit and activate other immune cells, and promote tissue damage.,,, (b) Microbicidal activity: M1 macrophages are equipped with potent microbicidal mechanisms, including the production of reactive oxygen species (ROS), reactive nitrogen species (RNS), and the expression of inducible nitric oxide synthase (iNOS)., These factors contribute to the killing of invading pathogens and tumor cells. (c) Antigen presentation: M1 macrophages upregulate the expression of class II molecules, enabling them to effectively present antigens to T cells and initiate adaptive immune responses., (d) Tissue remodeling: M1 macrophages secrete proteolytic enzymes, such as matrix metalloproteinases (MMPs), which contribute to the breakdown of extracellular matrix components, facilitating tissue remodeling and repair.,, M1 macrophages play crucial roles in the initial stages of inflammation, pathogen clearance, and tissue injury, coordinating the innate immune response and initiating the repair process.,,
M2 macrophages
In contrast to the proinflammatory M1 phenotype, M2 macrophages, also known as alternatively activated or anti‐inflammatory macrophages, are induced by exposure to cytokines such as IL‐4 and IL‐13 and immunomodulatory molecules like glucocorticoids and IL‐10.,,,,,,,, M2 macrophages are characterized by the expression of specific surface markers, including CD163 and CD206 (mannose receptor), and the production of anti‐inflammatory cytokines and mediators involved in tissue repair and homeostasis.,,, Key markers and functions of M2 macrophages include (a) anti‐inflammatory cytokine production: M2 macrophages secrete high levels of anti‐inflammatory cytokines such as IL‐10 and TGF‐β, which help to dampen the inflammatory response and promote tissue repair.,,,,, (b) Extracellular matrix remodeling: M2 macrophages contribute to synthesizing and remodeling extracellular matrix components, including collagen, fibronectin, and proteoglycans, facilitating tissue repair and wound healing.,, (c) Angiogenesis: M2 macrophages secrete proangiogenic factors, such as VEGF, which promote the formation of new blood vessels, ensuring adequate nutrient and oxygen supply to the injured tissue.,, (d) Phagocytosis and efferocytosis: M2 macrophages efficiently phagocytose cellular debris and apoptotic cells, a process known as efferocytosis, which is crucial for the resolution of inflammation and tissue remodeling.,,, (e) Tissue homeostasis: M2 macrophages play essential roles in maintaining tissue homeostasis by regulating metabolic processes, promoting insulin sensitivity, and contributing to the clearance of cellular debris.,, M2 macrophages are instrumental in the later stages of tissue repair, promoting the resolution of inflammation, angiogenesis, extracellular matrix remodeling, and restoring tissue homeostasis.,,
It is important to note that the M1/M2 polarization represents a continuum, and macrophages can exhibit a range of phenotypes between these two extremes, depending on the specific microenvironmental cues they encounter.,, Additionally, recent research has revealed the existence of distinct subpopulations within the M1 and M2 categories, each with unique transcriptional profiles and functional characteristics.,,, The dynamic interplay between M1 and M2 macrophages is crucial for orchestrating an effective immune response, balancing inflammation and tissue repair, and maintaining homeostasis. Dysregulation of this balance can contribute to the development and progression of various pathological conditions, including chronic inflammatory diseases, autoimmune disorders, and impaired wound healing.,, Understanding the molecular mechanisms governing macrophage polarization and the signaling pathways that regulate their phenotypic transformation is essential for developing targeted therapeutic strategies to modulate macrophage function and enhance tissue repair and regeneration.
The spectrum of macrophage activation states: beyond M1/M2 dichotomy
The advent of single‐cell technologies, such as single‐cell RNA sequencing (scRNA‐seq) and mass cytometry (CyTOF), has revolutionized our understanding of macrophage heterogeneity.,, These high‐resolution techniques have allowed researchers to profile the transcriptomes and proteomes of individual macrophages, uncovering a continuum of activation states that extend beyond the M1/M2 dichotomy. A seminal study by Xue et al. used scRNA‐seq to analyze human macrophages stimulated with 28 different activation conditions. They identified 49 distinct macrophage subsets, each with a unique transcriptional signature, highlighting the incredible diversity of macrophage responses to environmental cues. Similarly, a CyTOF study by Roussel et al. demonstrated that human macrophages exhibit a spectrum of activation states in response to various stimuli, with some cells coexpressing both M1 and M2 markers. Recent studies have also revealed novel macrophage subsets with unique functions. For example, Angel et al. identified a population of antigen‐presenting macrophages in human lymph nodes that express high levels of MHC class II and costimulatory molecules, suggesting a role in adaptive immunity. Another study by Zilionis et al. discovered a subset of mouse lung macrophages expressing M1 and M2 markers that play a critical role in maintaining lung homeostasis. These findings underscore the limitations of the M1/M2 classification system and emphasize the need for a more nuanced understanding of macrophage plasticity. The spectrum of activation states revealed by single‐cell technologies highlights the remarkable adaptability of macrophages to diverse environmental cues and their multifaceted roles in health and disease.,,
Tissue‐specific imprinting of macrophage identity and function
One of the most significant advances in macrophage biology over the past decade has been recognizing the profound influence of tissue microenvironments on macrophage development, phenotype, and function. Macrophages are present in virtually all tissues, performing specialized functions tailored to the unique demands of their local niche. Recent studies have shown that tissue‐specific factors, such as cytokines, metabolites, and cell–cell interactions, can imprint distinct transcriptional and epigenetic signatures on resident macrophages, giving rise to specialized subsets with unique functions., For example, Lavin et al. demonstrated that macrophages from different tissues, such as the lung, liver, and spleen, possess distinct enhancer landscapes shaped by tissue‐specific transcription factors. The gut microbiome has also emerged as a critical regulator of intestinal macrophage function., Studies have shown that microbial metabolites, such as short‐chain fatty acids and taurine, can modulate the phenotype and activity of intestinal macrophages, promoting homeostasis and protecting against enteric infections.,, These findings highlight the importance of studying macrophages in their native tissue context and underscore the limitations of extrapolating conclusions from in vitro studies to in vivo settings. The tissue‐specific imprinting of macrophage identity and function has important implications for our understanding of immune regulation and disease pathogenesis, as dysregulation of these processes may contribute to developing inflammatory and metabolic disorders.,,
Ontogenetic diversity of tissue‐resident macrophages
Another significant paradigm shift in macrophage biology has been the discovery of the ontogenetic diversity of tissue‐resident macrophages (TrMΦ)., Contrary to the traditional view that all tissue macrophages are derived from circulating monocytes, recent fate mapping studies have revealed that many TrMΦ are established during embryonic development and maintain themselves through local proliferation, independent of adult monocyte input., For example, microglia, the resident macrophages of the central nervous system, have been shown to originate from yolk sac‐derived progenitors that seed the brain early in embryonic development. Similarly, Kupffer cells, the resident macrophages of the liver, are derived from a combination of yolk sac and fetal liver progenitors. The ontogenetic origin of TrMΦ has important implications for their function and response to environmental challenges. Embryonically derived macrophages have been shown to possess unique transcriptional and epigenetic profiles compared with their monocyte‐derived counterparts, which may confer distinct functional properties., The discovery of the ontogenetic diversity of TrMΦ has also prompted a reevaluation of the contribution of monocyte‐derived macrophages to tissue homeostasis and inflammation. While monocyte‐derived macrophages play a crucial role in the response to injury and infection, their contribution to the maintenance of TrMΦ populations appears context dependent. It may vary across different organs and disease states.,
Trained immunity: long‐term reprogramming of macrophages
In addition to short‐term plasticity, macrophages can undergo long‐term functional reprogramming in response to microbial stimuli, known as trained innate immunity., This process involves epigenetic and metabolic changes that enhance the responsiveness of macrophages to subsequent challenges, providing a form of innate immune memory., A landmark study by Quintin et al. demonstrated that exposure to the fungal cell wall component β‐glucan induces epigenetic modifications in human monocytes, leading to increased production of proinflammatory cytokines upon restimulation. This trained immunity is mediated by changes in histone methylation, acetylation, and a metabolic shift toward glycolysis., Subsequent studies have shown that other microbial stimuli, such as the bacillus Calmette‐Guérin (BCG) vaccine and the bacterial component muramyl dipeptide, can also induce trained immunity in macrophages.,,, Arts et al. identified a critical role for ATF7 in mediating the epigenetic reprogramming of macrophages during β‐glucan‐induced training. Another study by Cheng et al. demonstrated that the metabolic enzyme glutamine synthetase is essential for the induction of trained immunity by β‐glucan, highlighting the link between metabolism and epigenetic reprogramming. The discovery of trained immunity has important implications for developing novel immunotherapies. For example, Moorlag et al. showed that BCG vaccination induces trained immunity in human monocytes, enhancing their ability to eliminate the respiratory syncytial virus. Harnessing trained immunity could be a promising strategy for boosting host defense against infectious diseases.
In summary, the study of macrophage plasticity has come a long way since the initial discovery of these versatile immune cells by Élie Metchnikoff in 1882. The traditional M1/M2 classification system provided a valuable framework for understanding macrophage polarization, but recent advances have revealed a spectrum of activation states that extend beyond this dichotomy. Single‐cell technologies have uncovered macrophages’ remarkable heterogeneity and ability to adapt to diverse tissue microenvironments. The functional significance of macrophage plasticity is evident in their roles in maintaining tissue homeostasis, orchestrating immune responses, and contributing to disease pathogenesis. Tissue‐specific imprinting and trained immunity further highlight the adaptability of macrophages to their local environment and their capacity for long‐term functional reprogramming.
SIGNALING PATHWAYS ORCHESTRATING MACROPHAGE POLARIZATION: AN INTRICATE REGULATORY NETWORK
Macrophages are versatile innate immune cells that play critical roles in host defense, tissue homeostasis, and disease pathogenesis. These cells exhibit remarkable plasticity, adapting their phenotype and function in response to diverse microenvironmental signals. Macrophage polarization refers to the process by which macrophages acquire distinct functional programs, classically categorized into two main subsets: classically activated (M1) and alternatively activated (M2) macrophages. M1 macrophages are induced by Th1 cytokines, such as IFN‐γ, and microbial products, including LPS. They exhibit potent proinflammatory and microbicidal activities, secreting high levels of proinflammatory cytokines (e.g., IL‐1β, IL‐6, IL‐12, and TNF‐α) and producing reactive oxygen and nitrogen species. In contrast, M2 macrophages are polarized by Th2 cytokines, such as IL‐4 and IL‐13, associated with anti‐inflammatory responses, tissue repair, and tumor progression. M2 macrophages produce anti‐inflammatory cytokines (e.g., IL‐10 and TGF‐β) and express scavenger receptors, mannose receptors, and ARG‐1. Recent studies have revealed that macrophage polarization is a highly dynamic and complex process involving the integration of multiple signaling pathways. These pathways are triggered by the engagement of PRRs, cytokine receptors, and other surface molecules, activating transcription factors and epigenetic regulators that shape the macrophage transcriptional landscape. Understanding the molecular mechanisms governing macrophage polarization is crucial for developing targeted therapies to modulate macrophage function in various pathological conditions, such as inflammatory diseases and cancer. This section provides an in‐depth discussion of the critical signaling pathways that orchestrate macrophage polarization, focusing on recent findings and their implications for therapeutic interventions. We will explore the roles of toll‐like receptors (TLRs), STAT proteins, nuclear receptors, miRNAs, metabolic reprogramming, and epigenetic modifications in shaping macrophage activation states. Furthermore, we will highlight the crosstalk between these signaling cascades and their potential as therapeutic targets for modulating macrophage function in disease contexts.
Toll‐like receptors: sentinels of macrophage polarization
TLRs are a family of pattern recognition receptors (PRRs) that play a pivotal role in the innate immune response by recognizing conserved molecular patterns associated with pathogens (PAMPs) and endogenous danger signals (DAMPs)., TLR signaling is a crucial driver of macrophage polarization, particularly in M1 activation.,, Engagement of TLRs by their respective ligands triggers the recruitment of adaptor proteins, such as myeloid differentiation primary response 88 (MyD88) and TIR‐domain‐containing adapter‐inducing IFN‐β (TRIF), which initiate downstream signaling cascades.,,, These cascades lead to the activation of transcription factors, including nuclear factor‐κB (NF‐κB), activator protein‐1 (AP‐1), and IFN regulatory factors (IRFs), which drive the expression of proinflammatory genes and shape the M1 macrophage phenotype.,,,,, TLR4, the receptor for bacterial LPS, is a potent inducer of M1 polarization., Upon LPS recognition, TLR4 activates both MyD88‐dependent and TRIF‐dependent pathways, producing proinflammatory cytokines and type I IFNs, respectively., The MyD88‐dependent pathway involves the activation of NF‐κB and mitogen‐activated protein kinases (MAPKs), such as p38, JNK, and ERK, which promote the expression of proinflammatory genes.,, The TRIF‐dependent pathway, on the other hand, activates IRF3 and IRF7, leading to the production of type I IFNs and the induction of IFN‐stimulated genes.,, Other TLRs, such as TLR2 (which recognizes bacterial lipoproteins) and TLR3 (which detects viral double‐stranded RNA), also contribute to macrophage polarization. TLR2 signaling predominantly activates NF‐κB and MAPKs, driving M1 polarization, while TLR3 activation leads to the production of type I IFNs and proinflammatory cytokines via the TRIF‐dependent pathway.,, Recent studies have revealed that TLR signaling can also modulate M2 polarization. For instance, activation of TLR2 and TLR4 has been shown to enhance the expression of M2 markers, such as ARG‐1 and Ym1, in the presence of IL‐4., This suggests that TLR signaling can fine‐tune macrophage polarization depending on the microenvironmental context and the presence of other polarizing stimuli. Targeting TLR signaling pathways has emerged as a promising therapeutic strategy for modulating macrophage polarization in various disease settings. For example, inhibition of TLR4 signaling has been shown to attenuate M1 polarization and promote M2‐like phenotypes in models of inflammatory diseases, such as rheumatoid arthritis and inflammatory bowel disease.,, Conversely, activation of TLR3 signaling has been explored to boost antitumor immunity by promoting M1 polarization in tumor‐associated macrophages (TAMs).,
STAT signaling: a key regulator of macrophage polarization
STAT proteins are transcription factors that play critical roles in cytokine signaling and macrophage polarization. Different STAT proteins are activated by specific cytokines and regulate distinct aspects of macrophage function, with STAT1 and STAT6 being particularly important for M1 and M2 polarization, respectively. STAT1 is activated by IFN‐γ, a potent inducer of M1 polarization., Upon IFN‐γ binding to its receptor, Janus kinases (JAKs) are activated, leading to the phosphorylation and dimerization of STAT1. Activated STAT1 dimers translocate to the nucleus, where they bind to gamma‐activated sequences in the promoters of target genes, driving the expression of proinflammatory and microbicidal factors, such as inducible iNOS and IL‐12., In contrast, STAT6 is activated by the Th2 cytokines IL‐4 and IL‐13, critical drivers of M2 polarization., Engagement of IL‐4 or IL‐13 with their respective receptors leads to the activation of JAKs and the phosphorylation of STAT6. Phosphorylated STAT6 dimers translocate to the nucleus and bind to specific DNA sequences, promoting the expression of M2‐associated genes, such as ARG‐1, mannose receptor (CD206), and resistin‐like molecule‐α (FIZZ1)., The balance between STAT1 and STAT6 activation is a critical determinant of macrophage polarization, with the relative abundance of IFN‐γ and IL‐4/IL‐13 in the microenvironment playing a key role., Interestingly, STAT1 and STAT6 have been shown to antagonize each other's functions, with STAT1 activation suppressing M2 polarization and STAT6 activation inhibiting M1 responses., This antagonism highlights the complex interplay between signaling pathways in shaping macrophage activation states. Targeting STAT signaling pathways has emerged as a potential therapeutic strategy for modulating macrophage polarization in various disease contexts. For example, inhibition of STAT1 signaling has been explored to attenuate M1 polarization and promote tissue repair in models of inflammatory diseases, such as multiple sclerosis and inflammatory bowel disease., Conversely, activation of STAT6 signaling has been investigated as a potential approach to promote M2 polarization and resolve inflammation in conditions such as obesity and atherosclerosis.,
Nuclear receptors: transcriptional regulators of macrophage polarization
Nuclear receptors are a family of ligand‐activated transcription factors that regulate macrophage polarization and function. Two nuclear receptors, peroxisome proliferator‐activated receptor‐γ (PPARγ) and liver X receptors (LXRs), have been particularly implicated in modulating macrophage activation states. PPARγ is a master regulator of M2 polarization, promoting the expression of anti‐inflammatory and tissue repair genes. Activation of PPARγ by endogenous ligands, such as polyunsaturated fatty acids and eicosanoids, or synthetic agonists, such as thiazolidinediones, leads to the formation of heterodimers with retinoid X receptors. These heterodimers bind to specific DNA sequences called PPAR response elements in the promoters of target genes, driving the expression of M2‐associated factors, such as ARG‐1, CD206, and IL‐10. PPARγ activation has been shown to antagonize M1 polarization by inhibiting the activity of proinflammatory transcription factors, such as NF‐κB and AP‐1. This antagonism is mediated through various mechanisms, including direct protein–protein interactions, competition for coactivators, and induction of anti‐inflammatory genes. Consequently, PPARγ agonists have been explored as potential therapeutic agents for modulating macrophage polarization in inflammatory diseases, such as atherosclerosis, obesity, and insulin resistance.,, LXRs, including LXRα and LXRβ, are another nuclear receptor class regulating macrophage polarization and function. LXRs are activated by oxysterols and oxidized cholesterol derivatives and play critical roles in lipid metabolism and inflammation. Activation of LXRs has been shown to promote an anti‐inflammatory M2‐like phenotype in macrophages, characterized by increased expression of genes involved in lipid efflux, such as ATP‐binding cassette transporters A1 and G1, and reduced production of proinflammatory cytokines., LXR agonists have demonstrated anti‐inflammatory and immunomodulatory effects in various disease models, including atherosclerosis, Alzheimer's, and autoimmune disorders., These effects are mediated, in part, by the ability of LXRs to inhibit NF‐κB signaling and promote the resolution of inflammation. As such, targeting LXR signaling has emerged as a potential therapeutic strategy for modulating macrophage polarization and function in inflammatory diseases.
MicroRNAs: posttranscriptional regulators of macrophage polarization
miRNAs are small noncoding RNAs that regulate gene expression at the posttranscriptional level by binding to complementary sequences in the 3′ untranslated regions of target mRNAs, leading to their degradation or translational repression.,, Evidence suggests that miRNAs play crucial roles in regulating macrophage polarization and function. Several miRNAs have been identified as key regulators of M1 polarization, including miR‐155, miR‐125b, and miR‐146a.,, miR‐155 is upregulated in M1 macrophages and promotes the expression of proinflammatory genes by targeting negative regulators of NF‐κB signaling, such as suppressor of cytokine signaling 1 (SOCS1) and Src homology 2 domain‐containing inositol‐5‐phosphatase 1., miR‐125b, on the other hand, inhibits M1 polarization by targeting the transcription factor IRF4, which is involved in the induction of proinflammatory cytokines. miR‐146a acts as a negative feedback regulator of M1 responses by targeting key components of the NF‐κB signaling pathway, such as IL‐1 receptor‐associated kinase 1 and TNF receptor‐associated factor 6. Similarly, several miRNAs have been implicated in regulating M2 polarization, including miR‐21, miR‐124, and miR‐223. miR‐21 promotes M2 polarization by targeting programmed cell death 4 (PDCD4), a negative regulator of IL‐10 production. miR‐124 is upregulated in M2 macrophages and promotes the expression of M2‐associated genes, such as ARG‐1 and FIZZ1, by targeting the transcription factor CCAAT/enhancer‐binding protein‐α. miR‐223 has been shown to promote M2 polarization by targeting Pknox1, a transcription factor that suppresses the expression of M2‐associated genes., The therapeutic potential of targeting miRNAs to modulate macrophage polarization has been explored in various disease models. For example, inhibition of miR‐155 has been shown to attenuate M1 polarization and promote M2‐like phenotypes in models of inflammatory diseases, such as rheumatoid arthritis and., Conversely, overexpression of miR‐21 or miR‐124 has been investigated to promote M2 polarization and resolve inflammation in conditions such as sepsis and spinal cord injury.
Metabolic regulation of macrophage polarization
Macrophage polarization is closely linked to metabolic reprogramming, with distinct metabolic profiles associated with M1 and M2 phenotypes.,, M1 macrophages rely on glycolysis and the pentose phosphate pathway to meet their energy demands and support their proinflammatory functions. In contrast, M2 macrophages primarily utilize oxidative phosphorylation and fatty acid oxidation for energy production. The mechanistic target of the rapamycin (mTOR) pathway is a central regulator of macrophage metabolism and polarization. mTOR complex 1 (mTORC1) is activated in M1 macrophages and promotes glycolysis through the induction of hypoxia‐inducible factor‐1α (HIF‐1α) and the expression of glycolytic enzymes.,,, Inhibition of mTORC1 by rapamycin or genetic deletion of its component Raptor skews macrophages toward an M2 phenotype. Adenosine monophosphate‐activated protein kinase (AMPK), a key energy sensor, is crucial in regulating macrophage polarization. AMPK activation promotes M2 polarization by inhibiting mTORC1 and enhancing oxidative metabolism., Metformin, an AMPK activator, has been shown to promote M2 polarization and alleviate inflammatory responses in various disease models., Recent studies have also highlighted the role of lipid metabolism in macrophage polarization. Fatty acid synthesis is upregulated in M1 macrophages, while fatty acid oxidation is associated with M2 polarization., PPARs, particularly PPARγ and PPARδ, are key regulators of lipid metabolism and have been implicated in promoting M2 polarization.
Epigenetic regulation of macrophage polarization
Epigenetic modifications, such as DNA methylation and histone modifications, are crucial in regulating macrophage polarization by modulating the accessibility of polarization‐associated genes., M1 and M2 macrophages exhibit distinct epigenetic signatures contributing to their phenotypic stability and plasticity. Histone deacetylases (HDACs) have emerged as essential regulators of macrophage polarization., HDAC3 has been shown to promote M1 polarization by deacetylating and activating NF‐κB, while its inhibition skews macrophages toward an M2 phenotype.,, In contrast, HDAC4 and HDAC5 have been implicated in promoting M2 polarization through the deacetylation of STAT6.,,, DNA methylation also plays a role in macrophage polarization. The DNA methyltransferase DNMT3b is upregulated in M1 macrophages and mediates the silencing of M2‐associated genes., Conversely, the demethylase TET2 promotes M2 polarization by demethylating and activating M2‐associated genes. Noncoding RNAs, such as miRNAs and long noncoding RNAs (lncRNAs), have also emerged as critical epigenetic regulators of macrophage polarization. For example, miR‐21 promotes M1 polarization by targeting the anti‐inflammatory cytokine IL‐10, while miR‐146a promotes M2 polarization by inhibiting NF‐κB signaling., LncRNAs, such as lncRNA‐Cox2 and lncRNA‐Mirt2, have been shown to regulate macrophage polarization by modulating the expression of polarization‐associated genes, (Table 2).
Polarization of macrophages in some pathological processes
Macrophage polarization is crucial in various physiological and pathological processes, including host defense, tissue homeostasis, inflammatory diseases, and cancer. Understanding the signaling pathways that govern macrophage polarization can provide valuable insights into disease pathogenesis and guide the development of targeted therapies. In inflammatory diseases, such as rheumatoid arthritis and inflammatory bowel disease, an imbalance between M1 and M2 macrophages contributes to chronic inflammation and tissue damage.,,, Targeting the signaling pathways that promote M1 polarization, such as TLR and NF‐κB signaling, has shown promise in alleviating inflammatory responses in preclinical models. Conversely, promoting M2 polarization through activating STAT6 or PPARγ has been explored as a strategy to resolve inflammation and promote tissue repair. In cancer, TAMs often exhibit an M2‐like phenotype and contribute to tumor progression by promoting angiogenesis, immunosuppression, and metastasis. Targeting the signaling pathways that drive M2 polarization in TAMs, such as colony‐stimulating factor (CSF)‐1/CSF‐1R and IL‐4/IL‐13 signaling, has emerged as a promising therapeutic approach., Reprogramming TAMs toward an M1‐like phenotype through TLR or STING signaling activation has also shown potential in enhancing antitumor immunity., In tissue regeneration and wound healing, M2 macrophages are crucial in promoting tissue repair and resolving inflammation. Harnessing the signaling pathways that promote M2 polarization, such as IL‐4/STAT6 and IL‐10/STAT3 signaling, has been explored to enhance tissue regeneration and limit fibrosis.,,
In summary, macrophage polarization is a dynamic and finely tuned process orchestrated by a complex network of signaling pathways. The integration of signals from TLRs, cytokines, and metabolic pathways shapes the functional phenotype of macrophages, allowing them to adapt to various microenvironmental cues. Recent advances in understanding the molecular mechanisms governing macrophage polarization have provided valuable insights into the role of these cells in health and disease. However, several challenges and opportunities remain in the field of macrophage polarization. The dichotomous M1/M2 classification, while applicable as a conceptual framework, oversimplifies the spectrum of macrophage activation states. Future studies should focus on delineating the complex heterogeneity of macrophage phenotypes and their functional implications in specific tissue contexts. Moreover, the crosstalk between signaling pathways and the influence of the tissue microenvironment on macrophage polarization warrants further investigation. Integrating multiomics approaches, such as transcriptomics, proteomics, and metabolomics, can provide a comprehensive understanding of the regulatory networks governing macrophage polarization. Translating the knowledge of macrophage polarization signaling into clinical applications remains a major challenge. Developing targeted therapies that modulate specific signaling pathways in macrophages while minimizing off‐target effects is crucial. Nanoparticle‐based drug delivery systems and engineered exosomes have shown promise in selectively targeting macrophages and modulating their polarization state.
MACROPHAGES: ORCHESTRATORS OF TISSUE REPAIR AND REGENERATION
Tissue injury triggers a highly coordinated cascade of events aimed at restoring tissue integrity and function. At the forefront of this intricate process are macrophages, versatile immune cells that exhibit remarkable plasticity and functional diversity. These cells play pivotal roles throughout the distinct phases of tissue repair and regeneration, seamlessly transitioning between proinflammatory and anti‐inflammatory phenotypes to facilitate the progression from initial injury to complete tissue restoration.
Initiation of the inflammatory response
The inflammatory phase is initiated by recognizing DAMPs and PAMPs by PRRs on macrophages and other immune cells., This recognition triggers a rapid phenotypic transformation of macrophages from a resting state to an activated, proinflammatory state, known as the M1 phenotype. The activation of M1 macrophages is mediated by a diverse array of PRRs, including TLRs, NLRs, and RLRs., TLRs, such as TLR4 and TLR2, are particularly crucial in this process, initiating signaling cascades that converge on the activation of transcription factors like NF‐κB and AP‐1, driving the expression of proinflammatory genes., Upon activation, M1 macrophages rapidly produce and secrete various proinflammatory cytokines and chemokines, including IL‐1β, IL‐6, IL‐12, IL‐23, and TNF‐α.,, These mediators orchestrate the inflammatory response, recruiting additional immune cells to the injury site and amplifying the inflammatory cascade.
Pathogen clearance and antimicrobial effector mechanisms
During the inflammatory phase, a primary function of M1 macrophages is the clearance of pathogens through various antimicrobial effector mechanisms. Phagocytosis, the process by which macrophages engulf and internalize pathogens or cellular debris, is a critical component of the innate immune response.,, M1 macrophages express receptors such as Fc and complement receptors, facilitating the recognition and binding of opsonized pathogens for efficient phagocytosis., Once internalized, pathogens are subjected to a range of intracellular killing mechanisms within the phagolysosome, a specialized compartment formed by the fusion of the phagosome with lysosomes. These mechanisms include: (a) ROS production: M1 macrophages generate a potent oxidative burst through the activity of NADPH oxidase, producing superoxide radicals and other ROS that can directly damage and kill pathogens., (b) NO production: iNOS in M1 macrophages catalyzes the production of NO, a highly reactive free radical that can directly kill or inhibit the growth of pathogens.,, (c) Antimicrobial peptides and enzymes: M1 macrophages produce antimicrobial peptides, such as defensins and cathelicidins, and lysosomal enzymes, like cathepsins and lysozymes, which can disrupt and degrade microbial cell walls and membranes.,, (d) Acidification: The phagolysosome provides an acidic environment, with a pH ranging from 4.5 to 5, which can directly inhibit the growth and survival of many pathogens., In addition to intracellular killing mechanisms, M1 macrophages employ extracellular strategies to combat pathogens, such as neutrophil extracellular trap formation, antimicrobial peptide and enzyme secretion, and cytokine and chemokine production to recruit and activate additional immune cells.,,,
Debris removal and tissue remodeling
M1 macrophages are crucial in removing cellular debris and initiating tissue remodeling during the inflammatory phase. They are essential for the clearance of apoptotic cells, a process known as efferocytosis, which prevents the release of potentially harmful intracellular contents and promotes the resolution of inflammation., Furthermore, M1 macrophages initiate the remodeling of the extracellular matrix (ECM) by producing proteolytic enzymes, such as MMPs, and cytokines that regulate ECM turnover. This ECM degradation facilitates the removal of damaged or necrotic tissue and creates space for the subsequent influx of new cells and the deposition of a provisional ECM., M1 macrophages also contribute to the initiation of angiogenesis, the formation of new blood vessels, by producing proangiogenic factors like VEGF, bFGF, and TNF‐α., These factors stimulate endothelial cell proliferation, migration, and the assembly of functional vascular structures (Figure 1).
Anti‐inflammatory signaling and resolution of inflammation
Following the initial inflammatory phase, the tissue repair process transitions into the proliferative and remodeling phases, characterized by the resolution of inflammation, angiogenesis, and ECM deposition and remodeling., During this stage, M2 macrophages, also known as alternatively activated or anti‐inflammatory macrophages, play a crucial role in orchestrating these processes and facilitating tissue regeneration. One of the critical functions of M2 macrophages is to promote the resolution of inflammation and create an environment conducive to tissue repair. They achieve this through the production of various anti‐inflammatory mediators and the suppression of proinflammatory pathways. M2 macrophages secrete anti‐inflammatory cytokines that counteract the proinflammatory effects of M1 macrophages and other immune cells. The primary anti‐inflammatory cytokine produced by M2 macrophages is IL‐10, which has potent immunosuppressive properties., IL‐10 inhibits the production of proinflammatory cytokines, such as TNF‐α, IL‐1β, and IL‐6, by M1 macrophages and other immune cells and downregulates the expression of MHC class II molecules and costimulatory molecules on antigen‐presenting cells, thereby suppressing the activation and proliferation of T cells.,, In addition to IL‐10, M2 macrophages produce TGF‐β, which has anti‐inflammatory and immunosuppressive effects. TGF‐β inhibits the activation and proliferation of T cells, suppresses the production of proinflammatory cytokines, and promotes the differentiation of regulatory T cells, which play a crucial role in maintaining immune homeostasis and resolving inflammation. M2 macrophages employ various mechanisms to suppress proinflammatory signaling pathways and attenuate the inflammatory response. One key mechanism is the upregulation of negative regulators of inflammation, such as SOCS proteins and A20 (TNFAIP3). SOCS proteins inhibit the JAK–STAT signaling pathway, which produces proinflammatory cytokines, while A20 negatively regulates the NF‐κB signaling pathway, a central regulator of inflammation.,, Additionally, M2 macrophages produce anti‐inflammatory lipid mediators, such as lipoxins, resolvins, and protectins, which can actively suppress proinflammatory signaling pathways and promote the clearance of apoptotic cells and debris.
Angiogenesis and vascular remodeling
M2 macrophages promote angiogenesis and vascular remodeling during tissue repair., They secrete various proangiogenic factors that stimulate endothelial cell proliferation, migration, and differentiation, facilitating the formation of new blood vessels. These factors include: (a) VEGF: a potent proangiogenic factor that induces endothelial cell proliferation, migration, and tube formation.,, (b) bFGF: stimulates endothelial cell proliferation and migration, as well as the production of proteolytic enzymes that facilitate cell invasion and ECM remodeling, essential processes for angiogenesis., (c) Placental growth factor: a member of the VEGF family that is crucial in promoting the recruitment and differentiation of endothelial progenitor cells, contributing to the formation of new blood vessels., (d) Angiopoietins: M2 macrophages produce angiopoietins, such as Ang‐1 and Ang‐2, which regulate the maturation, stabilization, and remodeling of newly formed blood vessels. In addition to producing proangiogenic factors, M2 macrophages can directly interact with endothelial cells and facilitate the formation of new blood vessels through a process known as vascular mimicry. This involves the physical association of M2 macrophages with endothelial cells, forming multicellular structures resembling vascular networks., M2 macrophages express adhesion molecules and receptors, such as integrin αvβ3 and the Tie2 receptor, mediating their interaction with endothelial cells and enabling the exchange of proangiogenic signals and the coordination of cellular processes involved in angiogenesis. Furthermore, M2 macrophages can transdifferentiate into endothelial‐like cells, directly contributing to forming new blood vessels. This transdifferentiation is mediated by various transcription factors, such as Prox1 and Coup‐TFII, which are involved in endothelial cell differentiation and vascular development.,
Extracellular matrix remodeling and tissue regeneration
The proliferation and remodeling phase is characterized by the deposition and remodeling of the ECM, a complex network of proteins and polysaccharides that provide structural support and signaling cues for cell migration, proliferation, and differentiation.,,,, M2 macrophages play a crucial role in regulating ECM remodeling and promoting tissue regeneration through the production of ECM components, regulation of ECM‐remodeling enzymes, and modulation of fibroblast and stem cell behavior.,,,
M2 macrophages contribute to the deposition and remodeling of the ECM by producing various ECM components, including: (a) Collagens: M2 macrophages secrete different types of collagens, such as collagen I, III, and IV, which are essential for the formation of the provisional ECM and the subsequent deposition of the mature ECM during tissue repair. (b) Fibronectin: a glycoprotein that plays a crucial role in cell adhesion, migration, and ECM assembly. M2 macrophages produce fibronectin, which helps create a provisional matrix for cell migration and proliferation during tissue repair. (c) Tenascin‐C: an ECM glycoprotein highly expressed during tissue repair that promotes cell migration, proliferation, and angiogenesis. M2 macrophages secrete tenascin‐C, which modulates the activity of various growth factors and cytokines, thereby regulating cellular processes in tissue regeneration., (d) GAGs: M2 macrophages produce various GAGs, such as hyaluronic acid, heparan sulfate, and chondroitin sulfate, essential ECM components. GAGs interact with growth factors, cytokines, and ECM proteins, modulating their activity and regulating cellular processes in tissue repair and regeneration., The deposition of a provisional ECM provides a scaffold for the recruitment and organization of various cell types, including endothelial cells, fibroblasts, and stem cells, enabling the formation of new tissue and restoring tissue integrity.,, Furthermore, the ECM components produced by M2 macrophages play a crucial role in modulating the behavior of other cells involved in tissue repair, such as cell migration, proliferation, and differentiation, through interactions with integrin receptors and the modulation of growth factor and cytokine activity.
M2 macrophages modulate the activity of various ECM‐remodeling enzymes, such as MMPs and tissue TIMPs, essential for ECM turnover and remodeling. During the proliferation and remodeling phase, M2 macrophages produce specific MMPs, such as MMP‐2 and MMP‐9, which facilitate the breakdown of existing ECM components, creating space for the deposition of new ECM and the migration of cells involved in tissue regeneration., However, excessive and uncontrolled MMP activity can lead to excessive ECM degradation and impair tissue repair. To maintain a balance between ECM degradation and deposition, M2 macrophages also produce TIMPs, which are endogenous inhibitors of MMPs. TIMPs bind to and inactivate MMPs, regulating their proteolytic activity and preventing excessive ECM breakdown., The production of specific MMPs and TIMPs by M2 macrophages is tightly controlled and depends on the stage of tissue repair and the microenvironmental cues present. For example, during the early stages of the proliferation and remodeling phase, M2 macrophages may produce higher levels of MMPs to facilitate the initial breakdown of the ECM and create space for new tissue formation., As the tissue repair process progresses, M2 macrophages may shift toward producing higher levels of TIMPs to stabilize the newly formed ECM and promote tissue maturation. In addition to regulating MMPs and TIMPs, M2 macrophages modulate the activity of other ECM‐remodeling enzymes, such as lysyl oxidases (LOXs) and transglutaminases. LOXs catalyze the cross‐linking of collagen and elastin fibers, increasing the stability and mechanical strength of the ECM. In contrast, transglutaminases catalyze the formation of covalent cross‐links between ECM proteins, further contributing to ECM stabilization and maturation,, (Figure 2).
Macrophage plasticity and phenotypic transitions
While the M1 and M2 phenotypes represent the extremes of the macrophage activation spectrum, it is crucial to recognize that macrophages exhibit a remarkable degree of plasticity, capable of adopting a wide range of functional states along a continuum. This plasticity allows macrophages to adapt dynamically to the changing microenvironmental cues encountered during tissue repair and regeneration.,, Recent studies have subdivided M2 macrophages into subgroups, including M2a, M2b, M2c, and M2d, based on their upstream activators and downstream gene expression patterns.,, For example, M2a macrophages are activated by IL‐4 and IL‐13, exhibiting increased expression of IL‐10, TGF‐β, and chemokines like CCL17, CCL18, and CCL22. In contrast, M2c macrophages are activated by glucocorticoids, IL‐10, and TGF‐β and exhibit increased transcription of IL‐10, TGF‐β, CCL16, and CCL18.,, This classification highlights macrophages’ complex nature and ability to modify their gene transcription profiles along a continuous spectrum, especially in pathological situations. It is important to note that the M1 and M2 phenotypes represent simplified extremes of a heterogeneous and dynamic functional continuum rather than distinct and mutually exclusive populations. Furthermore, macrophages can undergo phenotypic transitions in response to changing microenvironmental signals, allowing them to adapt their functional programs to the evolving needs of the tissue repair process. For example, M1 macrophages may transition to an M2‐like phenotype during the later stages of tissue repair, facilitating the resolution of inflammation and promoting tissue regeneration,, (Figure 3).
Macrophages in tissue‐specific repair and regeneration
While the general principles of macrophage involvement in tissue repair and regeneration are consistent across various organ systems, some tissue‐specific nuances and mechanisms highlight the versatility and adaptability of these cells. Here, we will briefly discuss the roles of macrophages in the repair and regeneration of selected tissues, including skeletal muscle, liver, heart, and skin.
Skeletal muscle repair and regeneration
In skeletal muscle injury, macrophages are crucial in coordinating the inflammatory response, promoting myogenesis, and facilitating tissue remodeling.,, M1 macrophages are the first to infiltrate the injured muscle, where they phagocytose debris and release proinflammatory cytokines to initiate the repair process., Subsequently, a phenotypic switch occurs, and M2 macrophages become predominant. These anti‐inflammatory macrophages secrete factors like IGF‐1 and TGF‐β that stimulate myoblast proliferation and differentiation.,, M2 macrophages also produce MMPs that degrade the extracellular matrix, allowing myoblast migration and fusion into multinucleated myotubes. Recent studies have revealed that macrophages can directly interact with muscle stem cells (satellite cells) through cell–cell contacts and paracrine signaling.,, These interactions regulate satellite cell quiescence, activation, proliferation, and differentiation, ensuring proper muscle regeneration. Furthermore, macrophages contribute to the revascularization of the regenerating muscle by producing proangiogenic factors like VEGF and promoting the formation of new blood vessels., This process is essential for delivering nutrients and oxygen to the newly formed muscle fibers.
Liver regeneration
The liver has a remarkable capacity for regeneration, and macrophages play a pivotal role in this process. Following partial hepatectomy or liver injury, Kupffer cells (liver‐resident macrophages) and infiltrating monocyte‐derived macrophages orchestrate the regenerative response.,, Initially, M1 macrophages promote hepatocyte proliferation by producing TNF‐α and IL‐6. They also phagocytose debris and apoptotic cells, creating space for the regenerating liver tissue.,, As regeneration progresses, M2 macrophages dominate and secrete factors like Wnt proteins, EGF, and MMPs that support hepatocyte proliferation, migration, and matrix remodeling.,, M2 macrophages also produce anti‐inflammatory cytokines like IL‐10 to resolve inflammation and prevent excessive tissue damage., Recent studies have highlighted the importance of macrophage–hepatocyte crosstalk in regulating liver regeneration. Macrophages respond to signals from hepatocytes and modulate their phenotype and function accordingly, creating a feedback loop that fine‐tunes the regenerative process.,
Cardiac repair and regeneration
While the adult mammalian heart has limited regenerative capacity, macrophages play a crucial role in regulating the inflammatory response and facilitating cardiac repair following myocardial infarction (MI)., After MI, M1 macrophages infiltrate the infarcted area and initiate the inflammatory response by producing proinflammatory cytokines and chemokines. They also phagocytose necrotic cardiomyocytes and debris, preparing the area for subsequent repair. As inflammation resolves, M2 macrophages become predominant and promote angiogenesis, extracellular matrix deposition, and scar formation. They secrete factors like VEGF, TGF‐β, and PDGF that stimulate endothelial cell proliferation, fibroblast activation, and collagen deposition., Interestingly, recent studies have suggested that macrophages may also play a role in cardiac regeneration by modulating the behavior of cardiac progenitor cells and cardiomyocytes., M2 macrophages can secrete factors like oncostatin M and IL‐33 that promote cardiomyocyte proliferation and survival, potentially contributing to new cardiac muscle., However, excessive inflammation and prolonged M1 macrophage activation can lead to adverse cardiac remodeling and heart failure., Therefore, modulating macrophage phenotypes and functions may represent a therapeutic strategy for improving cardiac repair and regeneration.
Skin wound healing
Macrophages are essential for proper skin wound healing, involving inflammation, tissue formation, and remodeling. During the inflammatory phase, M1 macrophages infiltrate the wound site and phagocytose pathogens, debris, and apoptotic cells. They also release proinflammatory cytokines and chemokines to recruit additional immune cells and initiate the repair process., As the inflammatory phase resolves, M2 macrophages become predominant and promote tissue formation and remodeling. They secrete growth factors like VEGF, TGF‐β, and PDGF that stimulate angiogenesis, keratinocyte migration and proliferation, and extracellular matrix deposition. M2 macrophages also play a role in wound contraction and scar formation by producing factors that activate fibroblasts and promote collagen deposition.,, Additionally, they secrete anti‐inflammatory cytokines like IL‐10 to resolve inflammation and prevent excessive tissue damage. Recent studies have highlighted the importance of macrophage‐keratinocyte crosstalk in regulating skin wound healing., Macrophages respond to signals from keratinocytes, modulate their phenotype, and function accordingly, creating a feedback loop that fine‐tunes the repair process.
Macrophage dynamics in chronic wounds
Chronic wounds, characterized by their persistent inflammatory state and impaired healing, pose a significant challenge in clinical settings. Among the various types of chronic wounds, diabetic wounds stand out as a significant concern due to their increasing prevalence and the unique microenvironment that hinders the healing process. In recent years, the role of macrophages in the pathogenesis and resolution of diabetic wounds has garnered significant attention., This section delves into the complex interplay between macrophages and the diabetic wound microenvironment, highlighting the mechanisms that influence macrophage phenotype and function and exploring potential therapeutic strategies targeting these interactions.
Diabetic wounds, particularly diabetic foot ulcers, are a common and severe complication of diabetes mellitus. The global prevalence of diabetic foot ulcers is estimated to be 6.3%, with a lifetime incidence of up to 25% among diabetic patients., These wounds are characterized by a prolonged inflammatory phase, impaired angiogenesis, and delayed re‐epithelialization, leading to a chronic nonhealing state. The unique microenvironment of diabetic wounds, shaped by hyperglycemia, oxidative stress, and the accumulation of advanced glycation end products (AGEs), significantly influences the behavior and function of macrophages, which are critical players in the wound healing process.,
The influence of the diabetic wound microenvironment on macrophage phenotype
In diabetic wounds, the local microenvironment is skewed toward factors promoting a persistent M1 phenotype, leading to chronic inflammation and impaired healing. High glucose levels, a hallmark of diabetes, have been shown to directly influence macrophage polarization. In vitro, studies have demonstrated that exposure to high glucose concentrations enhances the expression of proinflammatory cytokines, such as TNF‐α and IL‐1β, in macrophages while suppressing the expression of anti‐inflammatory markers, such as IL‐10 and ARG‐1., This shift toward an M1 phenotype is mediated through the activation of signaling pathways, including NF‐κB and MAPK, which are known to regulate inflammatory responses.,,
Oxidative stress, another key feature of the diabetic wound microenvironment, also plays a crucial role in modulating macrophage phenotype. ROS, such as superoxide and hydrogen peroxide, are elevated in diabetic wounds due to hyperglycemia‐induced mitochondrial dysfunction and the activation of NADPH oxidase., Excessive ROS levels contribute to the persistent activation of proinflammatory signaling cascades, such as the NF‐κB pathway, in macrophages., Moreover, ROS can directly damage macrophages, impairing their phagocytic function and ability to transition toward an M2 phenotype, which is essential for wound resolution.,
AGEs, formed by the nonenzymatic glycation of proteins and lipids under hyperglycemic conditions, accumulate in the diabetic wound bed and contribute to impaired healing., AGEs interact with their receptor (RAGE) on macrophages, triggering proinflammatory signaling pathways, such as NF‐κB and MAPK, and inducing the production of ROS and proinflammatory cytokines.,, The AGE–RAGE interaction also impairs macrophage efferocytosis, a process critical for the clearance of apoptotic cells and the resolution of inflammation. Consequently, the accumulation of AGEs in diabetic wounds perpetuates a state of chronic inflammation and hinders the transition of macrophages toward an M2 phenotype.
Mechanisms underlying the effects of glucose, ROS, and AGEs on macrophages
The mechanisms by which high glucose, ROS, and AGEs influence macrophage function in diabetic wounds are complex and multifaceted. High glucose levels can directly alter macrophage metabolism, shifting it toward a more glycolytic phenotype associated with the M1 polarization state., This metabolic reprogramming is mediated through the activation of HIF‐1α and the upregulation of glycolytic enzymes, such as hexokinase and pyruvate kinase,, The increased glycolytic flux in macrophages promotes the production of proinflammatory cytokines and impairs their ability to engage in oxidative phosphorylation, which is necessary for the M2 phenotype.
Oxidative stress, driven by elevated ROS levels, contributes to the persistent activation of redox‐sensitive transcription factors, such as NF‐κB and AP‐1, in macrophages., These transcription factors regulate the expression of proinflammatory genes, including TNF‐α, IL‐1β, and IL‐6, perpetuating the inflammatory response in diabetic wounds. ROS can also directly damage macrophages by inducing lipid peroxidation, protein carbonylation, and DNA damage, impairing their function and survival.,, Furthermore, ROS‐mediated oxidative modifications of proteins can generate new AGEs, amplifying the AGE–RAGE signaling loop and exacerbating inflammation.
AGEs interact with RAGE on macrophages, triggering a cascade of signaling events that promote the M1 phenotype., The AGE–RAGE interaction activates NF‐κB and MAPK pathways, leading to the transcription of proinflammatory genes and the production of ROS. Additionally, AGEs can induce epigenetic modifications in macrophages, such as histone acetylation and DNA methylation, which regulate gene expression in inflammation and wound healing., For example, AGEs have been shown to increase the acetylation of histone H3 at the promoter regions of proinflammatory genes, such as TNF‐α and IL‐1β, enhancing their transcription. AGEs also impair macrophage efferocytosis by downregulating the expression of efferocytosis receptors, such as MerTK and CD36, and by inducing the production of “don't eat me” signals, such as CD47, on apoptotic cells.,
Targeting macrophage‐microenvironment interactions for diabetic wound treatment
Understanding the complex interactions between macrophages and the diabetic wound microenvironment provides valuable insights for developing targeted therapeutic strategies. One promising approach is modulating the ROS levels in the wound bed. Antioxidants, such as N‐acetylcysteine and vitamin E, have reduced oxidative stress and improved wound healing in diabetic animal models.,, These antioxidants scavenge ROS, attenuate the activation of proinflammatory signaling pathways, and promote the polarization of macrophages toward an M2 phenotype. Clinical studies have also demonstrated the potential of topical antioxidant application in improving diabetic wound healing, highlighting the translational relevance of targeting ROS.,
Another strategy is inhibiting AGE formation and accumulation of AGEs in the wound bed. Pharmacological agents, such as aminoguanidine and pyridoxamine, have been shown to reduce AGE formation and improve wound healing in diabetic animal models., These compounds trap reactive carbonyl intermediates and prevent their condensation with proteins to form AGEs. Additionally, targeting the AGE–RAGE signaling axis using RAGE antagonists or soluble RAGE (sRAGE) has shown promise in preclinical studies. sRAGE acts as a decoy receptor, sequestering AGEs and preventing their interaction with cell surface RAGE, thus attenuating proinflammatory signaling in macrophages.,
Modulating macrophage metabolism is another potential therapeutic approach. Compounds that promote oxidative phosphorylation and mitochondrial biogenesis, such as resveratrol and metformin, have been shown to skew macrophages toward an M2 phenotype and improve wound healing in diabetic animal models.,,, These compounds activate AMPK to promote the expression of anti‐inflammatory genes and suppress glycolysis. Clinical trials investigating the effects of metformin on diabetic wound healing have shown promising results, with improved wound closure rates and reduced inflammation.
In conclusion, macrophages are versatile and dynamic cells that play pivotal roles throughout the various tissue repair and regeneration phases. Their remarkable plasticity and ability to adapt to changing microenvironmental cues allow them to orchestrate various processes, from initiating inflammation and pathogen clearance to promoting angiogenesis, extracellular matrix remodeling, and tissue regeneration. As our understanding of macrophage biology continues to deepen, these cells hold great promise as therapeutic targets for enhancing tissue repair and regenerative processes in various pathological conditions.
HARNESSING MACROPHAGES: TARGETING PATHWAYS FOR TISSUE REPAIR AND REGENERATION
Macrophages, the versatile cells of the innate immune system, have emerged as pivotal players in the intricate tissue repair and regeneration process. Recent advancements in regenerative medicine and molecular biology have shed light on the critical role of macrophages in promoting the regeneration of various tissues, including the heart, liver, kidney, muscle, and nerves. The ability of macrophages to adopt diverse phenotypes in response to microenvironmental cues has made them attractive therapeutic targets for enhancing tissue repair and regeneration. This section explores the current strategies for harnessing macrophages to promote tissue repair and regeneration, focusing on the latest research findings from the past decade. We discuss targeting specific pathways, such as the CSF‐1/CSF‐1R signaling pathway, and the modulation of macrophage function through signaling pathways and transcription factors. Additionally, we highlight the potential of relay transfer and cell transplantation of macrophages and biomaterial‐based strategies for precise regulation of macrophage polarization phenotypes (Figure 4).
Targeting the CSF‐1/CSF‐1R signaling pathway
The macrophage CSF‐1 and its receptor (CSF‐1R) signaling pathway play a crucial role in the maturation and transformation of TrMΦ, making it an attractive target for therapeutic,,, interventions. Stutchfield et al. demonstrated that the administration of CSF1‐Fc, an exogenous form of CSF‐1, enhanced the recruitment and conversion of monocytes into protective hepatic macrophages, facilitating liver recovery after acute injury and partial hepatectomy. Furthermore, a systematic review and meta‐analysis by Wei et al. provided robust evidence supporting the efficacy and safety of CSF in accelerating wound healing. In addition to CSF‐related approaches, targeting chemokine receptors on monocytes and macrophages has shown promise in altering their migration patterns and impacting their function in tissue repair., Promoting the survival of M2 macrophages, which play an essential role in tissue repair and angiogenesis, represents another promising strategy for enhancing tissue healing.
Modulating macrophage function through signaling pathways and transcription factors
Manipulating macrophage function by targeting specific signaling pathways and transcription factors has emerged as a promising therapeutic strategy for promoting tissue repair and regeneration. The TLR9 signaling pathway has been found to encourage macrophage M2 polarization in various models. Activation of the TLR9 pathway, such as with the agonist cobitolimod, induces a prohealing phenotype in macrophages, enhancing macrophage‐mediated tissue healing in conditions like ulcerative colitis. Transcription factors, including NF‐κB and MAPK, play critical roles in macrophage activation and polarization., Inhibiting these signaling pathways has shown promising results in promoting M2 polarization and reducing inflammation. Puerarin, a compound from traditional Chinese medicine, has demonstrated the ability to inhibit NF‐κB and MAPK pathways, leading to decreased production of inflammatory cytokines and promotion of M2 polarization in macrophages.,, Noncoding RNAs, particularly miRNAs, have also emerged as important macrophage polarization and activation regulators. Targeting specific noncoding RNAs provides a means to modulate macrophage function and influence tissue repair processes., For instance, inhibiting the pro‐M1 polarization molecule CRMP2 through small interfering RNA has demonstrated reduced local inflammation and fibrosis following MI.
Relay transfer and cell transplantation of macrophages
Targeting specific subpopulations of macrophages through relay transfer and cell transplantation has shown great potential for clinical treatment aimed at tissue repair and regeneration. Lopes et al. demonstrated the efficacy of modifying macrophages to express the M2 phenotype in vitro and subsequently transferring these M2 macrophages to a colitis mouse model, reducing inflammation and pathological damage. Similarly, Zheng et al. stimulated macrophages to adopt the M2 phenotype using IL‐4 and IL‐13. They transplanted these M2 macrophages into a streptozotocin‐induced diabetic mouse model, significantly reducing damage in the islets and kidneys. These studies highlight the potential of relay transfer and polarized macrophage cell transplantation to promote tissue repair and regeneration. However, further research is needed to fully understand the mechanisms of macrophage polarization and develop more precise and effective strategies for modulating macrophage function in vivo. This includes identifying specific markers and signaling pathways that regulate macrophage polarization and investigating methods to optimize the survival and functionality of transplanted macrophages.
Biomaterial‐based strategies for precise regulation of macrophage polarization
Recent advancements in biomaterials have enabled precise regulation of macrophage polarization phenotypes, specifically M1/M2, leading to enhanced tissue regeneration and accelerated wound healing.,,,,, Hydrogel‐based constructs, known for their biocompatibility, tunable physical properties, and drug‐delivery capabilities, have emerged as valuable tools for tissue repair.,, Huang et al. developed curcumin‐based metal‐organic framework hydrogels that effectively downregulated M1 macrophage‐related gene expression while upregulating anti‐inflammatory gene expression, promoting the polarization of macrophages toward the M2 phenotype and facilitating the regeneration of blood vessels and nerves in chronic wounds. Henn et al. investigated xenotransplantation‐mediated activation of Trem2+ macrophages, which promoted re‐epithelialization and angiogenesis through growth factor secretion and contributed to collagen remodeling by secreting MMPs. By designing a soft pullulan‐collagen hydrogel, delivery of Trem2+ macrophages obtained after vitamin D3 treatment to the wound bed showed great potential for clinical translation. Biomaterials offer a platform for precise modulation of macrophage function and polarization through tailored design and incorporation of specific cues, such as drug delivery systems or bioactive molecules.,,, Further research is needed to optimize the design and functionality of biomaterials to achieve better control over macrophage polarization and ultimately improve clinical outcomes in tissue repair and regeneration (Table 3).
Therapeutic potential and clinical applications
The therapeutic potential of macrophages in cell‐based therapies has been demonstrated in various clinical trials and preclinical studies.,, Macrophages have outperformed stem cells in specific target diseases, showcasing their outstanding regenerative capacity. Conditions such as kidney disease, stroke, arterial disease, and cancer have been targeted using macrophage‐based therapies. Genetic modification of macrophages, such as the development of chimeric antigen receptor‐macrophages (CAR‐M), has further expanded the potential of genetically engineered macrophages for cell therapy.,, The use of induced pluripotent stem cell (iPSC)‐derived macrophages, macrophages loaded with nanoparticles, ex vivo polarization and adoptive transfer of macrophages, and surface‐anchoring engineering of macrophages have also shown promising results in preclinical studies.,, The therapeutic applications of macrophage CSF‐1 have been explored in various contexts, including tissue repair after ischemia in the kidney and heart, promotion of angiogenesis, and elimination of amyloid deposits in the brain.,, CSF‐1 has been shown to promote a resident‐type macrophage phenotype, making it a potential treatment for tissue repair (Table 4).
In summary, macrophages play a crucial role in tissue repair, regeneration, and fibrosis, making them attractive targets for therapeutic interventions. The ability to harness macrophages through various strategies, such as targeting specific signaling pathways, modulating macrophage function, relay transfer and cell transplantation, and biomaterial‐based approaches, holds great promise for enhancing tissue repair and regeneration. Future research should further elucidate the mechanisms that instruct macrophages to adopt specific phenotypes and identify novel targets for therapeutic modulation. The development of more precise and effective strategies for modulating macrophage function in vivo and optimizing the survival and functionality of transplanted macrophages will be crucial for translating these findings into clinical applications. Additionally, the potential of genetically engineered macrophages, such as CAR‐M, and using iPSC‐derived macrophages warrant further exploration. Combining macrophage‐based therapies with other therapeutic modalities, such as biomaterials and drug delivery systems, may also provide synergistic effects and improve clinical outcomes.
CONCLUSION AND PROSPECTS
Macrophages are remarkably plastic cells that play pivotal roles in tissue homeostasis, inflammation, repair, and regeneration. The past decade has witnessed significant advances in understanding the molecular mechanisms governing macrophage plasticity and their functional implications in health and disease. While providing a helpful framework, the traditional M1/M2 classification system has been challenged by the emergence of a spectrum of activation states revealed by single‐cell technologies. The complex interplay between tissue‐specific factors, ontogeny, and microenvironmental cues shapes macrophages’ transcriptional and epigenetic landscape, giving rise to a diverse array of functional phenotypes. The signaling pathways orchestrating macrophage polarization have been extensively studied, with TLRs, STAT proteins, nuclear receptors, and miRNAs emerging as key regulators. The integration of these signaling cascades, along with metabolic reprogramming and epigenetic modifications, fine‐tunes macrophage responses to various stimuli. Notably, the crosstalk between these pathways and the influence of the tissue microenvironment on macrophage plasticity has been increasingly recognized. The discovery of TrMΦ with distinct ontogenies and the concept of trained immunity have further expanded our understanding of macrophage heterogeneity and their capacity for long‐term functional reprogramming. The functional significance of macrophage plasticity is exemplified by their roles in tissue repair and regeneration. Macrophages orchestrate the inflammatory response, clear cellular debris, and promote angiogenesis, extracellular matrix remodeling, and tissue regeneration. The dynamic transition from proinflammatory to proresolving phenotypes is crucial for successfully executing the repair process. Dysregulation of macrophage function contributes to impaired wound healing, fibrosis, and chronic inflammation, underscoring the therapeutic potential of targeting macrophage polarization in various pathological conditions.
Despite the significant progress in understanding macrophage plasticity, several challenges and opportunities remain. The complex heterogeneity of macrophage phenotypes in vivo and their functional implications in specific tissue contexts warrant further investigation. Developing more sophisticated computational tools and spatial transcriptomics approaches will enable a more comprehensive analysis of macrophage diversity and its interactions with other cells in the tissue microenvironment. Moreover, the mechanisms underlying the crosstalk between signaling pathways and the long‐term epigenetic reprogramming of macrophages in response to environmental challenges require further elucidation. Translating the knowledge of macrophage plasticity into clinical applications is a significant challenge and opportunity. Targeting specific signaling pathways or transcription factors to modulate macrophage function holds promise for treating inflammatory diseases, fibrotic disorders, and impaired wound healing. However, developing targeted therapies that selectively modulate macrophage polarization while minimizing off‐target effects remains a significant hurdle. Nanoparticle‐based drug delivery systems and engineered exosomes have shown potential in delivering therapeutic agents specifically to macrophages, but their clinical translation requires further optimization and safety evaluation. The field of macrophage‐based cell therapies is rapidly evolving, with strategies such as adoptive transfer of ex vivo polarized macrophages, genetic engineering of macrophages, and the use of iPSC‐derived macrophages showing promising results in preclinical studies. However, these engineered macrophages’ long‐term survival, functionality, and safety in vivo need to be carefully assessed. Combining macrophage‐based therapies with other therapeutic modalities, such as biomaterials, growth factors, and immunomodulatory agents, may provide synergistic effects and improve clinical outcomes.
In conclusion, macrophage plasticity is a fundamental property that underlies their diverse functions in tissue homeostasis, inflammation, repair, and regeneration. The past decade has witnessed a paradigm shift in understanding macrophage heterogeneity and the molecular mechanisms governing their polarization. Integrating single‐cell technologies, spatial transcriptomics, and computational approaches has unveiled the complex landscape of macrophage activation states and their functional implications. Targeting macrophage plasticity holds immense therapeutic potential for various diseases, from inflammatory disorders to tissue regeneration and cancer. However, translating these findings into clinical applications requires a deeper understanding of the context‐dependent roles of macrophages, the development of more precise and effective strategies for modulating their function, and rigorous safety and efficacy evaluations. As the field of macrophage biology continues to evolve, interdisciplinary collaborations between immunologists, bioengineers, and clinicians will be crucial in harnessing the power of these versatile cells to benefit human health. With the rapid pace of scientific discoveries and technological advancements, the coming years promise to be an exciting era for macrophage research, with the potential to revolutionize our approach to treating diseases and promoting tissue regeneration.
AUTHOR CONTRIBUTIONS
Lingfeng Yan and Jue Wang wrote the manuscript and drew the figures. Xin Cai helped design the tables. Yih‐Cherng Liou, Han‐Ming Shen, and Jianlei Hao helped design the manuscript structure and write the manuscript. Canhua Huang, Gaoxing Luo, and Weifeng He evaluated and reviewed the manuscript structure, ideas and science. All authors have read and approved the final manuscript.
CONFLICT OF INTEREST STATEMENT
Author Canhua Huang and Yih‐Cherng Liou are Editorial board members of Medcomm. Author Canhua Huang and Yih‐Cherng Liou were not involved in the journal's review of or decisions related to this manuscript. The other authors declared no conflict of interest.
ETHICS STATEMENT
No ethical approval was required for this study.
References 581
- 1.
- 2.
- 3.
Kloc M, Ghobrial RM, Wosik J, Lewicka A, Lewicki S, Kubiak JZ. Macrophage functions in wound healing. J Tissue Eng Regen Med. 2019;13(1):99‐109.
Not in our library10.1002/term.2772
- 4.
Chen C, Liu T, Tang Y, Luo G, Liang G, He W. Epigenetic regulation of macrophage polarization in wound healing. Burns Trauma. 2023;11:tkac057.
Not in our library10.1093/burnst/tkac057
- 5.
- 6.
Sun X, Li Y, Deng Q, et al. Macrophage polarization, metabolic reprogramming, and inflammatory effects in ischemic heart disease. Front Immunol. 2022;13:934040.
Not in our library10.3389/fimmu.2022.934040
- 7.
Willenborg S, Sanin DE, Jais A, et al. Mitochondrial metabolism coordinates stage‐specific repair processes in macrophages during wound healing. Cell Metab. 2021;33(12):2398‐2414. e9.
Not in our library10.1016/j.cmet.2021.10.004
- 8.
- 9.
Funes SC, Rios M, Escobar‐Vera J, Kalergis AM. Implications of macrophage polarization in autoimmunity. Immunology. 2018;154(2):186‐195.
Not in our library10.1111/imm.12910
- 10.
Mantovani A, Sica A, Locati M. Macrophage polarization comes of age. Immunity. 2005;23(4):344‐346.
Not in our library10.1016/j.immuni.2005.10.001
- 11.
Karlinsey K, Qu L, Matz AJ, Zhou B. A novel strategy to dissect multifaceted macrophage function in human diseases. J Leukoc Biol. 2022;112(6):1535‐1542.
Not in our library10.1002/jlb.6mr0522-685r
- 12.
An L, Michaeli J, Pallavi P, et al. Concurrent stimulation of monocytes with CSF1 and polarizing cytokines reveals phenotypic and functional differences with classical polarized macrophages. J Leukoc Biol. 2022;112(3):437‐447.
Not in our library10.1002/jlb.3a0721-383r
- 13.
O'Brien EM, Spiller KL. Pro‐inflammatory polarization primes Macrophages to transition into a distinct M2‐like phenotype in response to IL‐4. J Leukoc Biol. 2022;111(5):989‐1000.
Not in our library10.1002/jlb.3a0520-338r
- 14.
Liang B, Wang H, Wu D, Wang Z. Macrophage M1/M2 polarization dynamically adapts to changes in microenvironment and modulates alveolar bone remodeling after dental implantation. J Leukoc Biol. 2021;110(3):433‐447.
Not in our library10.1002/jlb.1ma0121-001r
- 15.
Mills CD, Kincaid K, Alt JM, Heilman MJ, Hill AM. M‐1/M‐2 macrophages and the Th1/Th2 paradigm. J Immunol. 2000;164(12):6166‐6173.
Not in our library10.4049/jimmunol.164.12.6166
- 16.
Eming SA, Murray PJ, Pearce EJ. Metabolic orchestration of the wound healing response. Cell Metab. 2021;33(9):1726‐1743.
Not in our library10.1016/j.cmet.2021.07.017
- 17.
He P, Dai M, Li Z, et al. Effect of connexin 43 in LPS/IL‐4‐induced macrophage M1/M2 polarization: an observational study. Medicine (Baltimore). 2024;103(15):e37811.
Not in our library10.1097/md.0000000000037811
- 18.
Scott TE, Lewis CV, Zhu M, et al. IL‐4 and IL‐13 induce equivalent expression of traditional M2 markers and modulation of reactive oxygen species in human macrophages. Sci Rep. 2023;13(1):19589.
Not in our library10.1038/s41598-023-46237-2
- 19.
Zhu Y, Chen X, Lu Y, et al. Glutamine mitigates murine burn sepsis by supporting macrophage M2 polarization through repressing the SIRT5‐mediated desuccinylation of pyruvate dehydrogenase. Burns Trauma. 2022;10:tkac041.
Not in our library10.1093/burnst/tkac041
- 20.
- 21.
Oliver MA, Davis XD, Bohannon JK. TGFβ macrophage reprogramming: a new dimension of macrophage plasticity. J Leukoc Biol. 2024;115(3):411‐414.
Not in our library10.1093/jleuko/qiae001
- 22.
Wynn TA, Vannella KM. Macrophages in Tissue Repair, Regeneration, and Fibrosis. Immunity. 2016;44(3):450‐462.
Not in our library10.1016/j.immuni.2016.02.015
- 23.
- 24.
Gordon S. Phagocytosis: the legacy of Metchnikoff. Cell. 2016;166(5):1065‐1068.
Not in our library10.1016/j.cell.2016.08.017
- 25.
Life of Elie Metchnikoff, 1845–1916. Nature. 1922;109(2728):163‐166.
Not in our library
- 26.
Van Epps HL. Macrophage activation unveiled. J Exp Med. 2005;202(7):884.
Not in our library10.1084/jem.2027fta
- 27.
- 28.
Wlaschek M, Singh K, Sindrilaru A, Crisan D, Scharffetter‐Kochanek K. Iron and iron‐dependent reactive oxygen species in the regulation of macrophages and fibroblasts in non‐healing chronic wounds. Free Radic Biol Med. 2019;133:262‐275.
Not in our library10.1016/j.freeradbiomed.2018.09.036
- 29.
- 30.
- 31.
Mackaness GB, Blanden RV. Cellular immunity. Prog Allergy. 1967;11:89‐140.
Not in our library
- 32.
Stein M, Keshav S, Harris N, Gordon S. Interleukin 4 potently enhances murine macrophage mannose receptor activity: a marker of alternative immunologic macrophage activation. J Exp Med. 1992;176(1):287‐292.
Not in our library10.1084/jem.176.1.287
- 33.
von Recklinghausen F. Ueber Eiter‐ und Bindegewebskörperchen. Arch Pathol Anat Physiol Klin Med. 1863;28(1):157‐197.
Not in our library
- 34.
Tauber AI. Metchnikoff and the phagocytosis theory. Nat Rev Mol Cell Biol. 2003;4(11):897‐901.
Not in our library10.1038/nrm1244
- 35.
Sródka A, Gryglewski RW, Szczepariski W. Browicz or Kupffer cells? Pol J Pathol. 2006;57(4):183‐185.
Not in our library
- 36.
Aschoff L. Das reticuloendotheliale System. Ergebn Inn Med Kinderheilk. 1924;26:1‐118.
Not in our library
- 37.
van Furth R, Cohn ZA. The origin and kinetics of mononuclear phagocytes. J Exp Med. 1968;128(3):415‐435.
Not in our library10.1084/jem.128.3.415
- 38.
van Furth R. Current view on the mononuclear phagocyte system. Immunobiology. 1982;161(3‐4):178‐185.
Not in our library10.1016/s0171-2985(82)80072-7
- 39.
Quintin J, Saeed S, Martens JHA, et al. Candida albicans infection affords protection against reinfection via functional reprogramming of monocytes. Cell Host Microbe. 2012;12(2):223‐232.
Not in our library10.1016/j.chom.2012.06.006
- 40.
Lavin Y, Winter D, Blecher‐Gonen R, et al. Tissue‐resident macrophage enhancer landscapes are shaped by the local microenvironment. Cell. 2014;159(6):1312‐1326.
Not in our library10.1016/j.cell.2014.11.018
- 41.
- 42.
Cheng SC, Quintin J, Cramer RA, et al. mTOR‐ and HIF‐1α‐mediated aerobic glycolysis as metabolic basis for trained immunity. Science. 2014;345(6204):1250684.
Not in our library10.1126/science.1250684
- 43.
Arts RJ, Novakovic B, Ter Horst R, et al. Glutaminolysis and fumarate accumulation integrate immunometabolic and epigenetic programs in trained immunity. Cell Metab. 2016;24(6):807‐819.
Not in our library10.1016/j.cmet.2016.10.008
- 44.
Roussel M, Ferrell PB, Jr., Greenplate AR, et al. Mass cytometry deep phenotyping of human mononuclear phagocytes and myeloid‐derived suppressor cells from human blood and bone marrow. J Leukoc Biol. 2017;102(2):437‐447.
Not in our library10.1189/jlb.5ma1116-457r
- 45.
Zilionis R, Engblom C, Pfirschke C, et al. Single‐cell transcriptomics of human and mouse lung cancers reveals conserved myeloid populations across individuals and species. Immunity. 2019;50(5):1317‐1334. e10.
Not in our library10.1016/j.immuni.2019.03.009
- 46.
- 47.
Wu MM, Wang QM, Huang BY, et al. Dioscin ameliorates murine ulcerative colitis by regulating macrophage polarization. Pharmacol Res. 2021;172:105796.
Not in our library10.1016/j.phrs.2021.105796
- 48.
Lin YH, Wang YH, Peng YJ, et al. Interleukin 26 skews macrophage polarization towards M1 phenotype by activating cJUN and the NF‐κB pathway. Cells. 2020;9(4):938.
Not in our library10.3390/cells9040938
- 49.
Liu L, Stokes JV, Tan W, Pruett SB. An optimized flow cytometry panel for classifying macrophage polarization. J Immunol Methods. 2022;511:113378.
Not in our library10.1016/j.jim.2022.113378
- 50.
Zhang J, Liu X, Wan C, et al. NLRP3 inflammasome mediates M1 macrophage polarization and IL‐1β production in inflammatory root resorption. J Clin Periodontol. 2020;47(4):451‐460.
Not in our library10.1111/jcpe.13258
- 51.
Hirani D, Alvira CM, Danopoulos S, et al. Macrophage‐derived IL‐6 trans‐signalling as a novel target in the pathogenesis of bronchopulmonary dysplasia. Eur Respir J. 2022;59(2):2002248.
Not in our library10.1183/13993003.02248-2020
- 52.
- 53.
Shapouri‐Moghaddam A, Mohammadian S, Vazini H, et al. Macrophage plasticity, polarization, and function in health and disease. J Cell Physiol. 2018;233(9):6425‐6440.
Not in our library10.1002/jcp.26429
- 54.
Zhang B, Yang Y, Yi J, Zhao Z, Ye R. Hyperglycemia modulates M1/M2 macrophage polarization via reactive oxygen species overproduction in ligature‐induced periodontitis. J Periodontal Res. 2021;56(5):991‐1005.
Not in our library10.1111/jre.12912
- 55.
Rendra E, Riabov V, Mossel DM, Sevastyanova T, Harmsen MC, Kzhyshkowska J. Reactive oxygen species (ROS) in macrophage activation and function in diabetes. Immunobiology. 2019;224(2):242‐253.
Not in our library10.1016/j.imbio.2018.11.010
- 56.
Fan X, Zheng S, Chen C, et al. Sialidase facilitates Porphyromonas gingivalis immune evasion by reducing M1 polarization, antigen presentation, and phagocytosis of infected macrophages. Front Cell Infect Microbiol. 2023;13:1173899.
Not in our library10.3389/fcimb.2023.1173899
- 57.
Mohammadi A, Blesso CN, Barreto GE, Banach M, Majeed M, Sahebkar A. Macrophage plasticity, polarization and function in response to curcumin, a diet‐derived polyphenol, as an immunomodulatory agent. J Nutr Biochem. 2019;66:1‐16.
Not in our library10.1016/j.jnutbio.2018.12.005
- 58.
Bogen B, Fauskanger M, Haabeth OA, Tveita A. CD4(+) T cells indirectly kill tumor cells via induction of cytotoxic macrophages in mouse models. Cancer Immunol Immunother. 2019;68(11):1865‐1873.
Not in our library10.1007/s00262-019-02374-0
- 59.
Zhang H, Cai D, Bai X. Macrophages regulate the progression of osteoarthritis. Osteoarthritis Cartilage. 2020;28(5):555‐561.
Not in our library10.1016/j.joca.2020.01.007
- 60.
Ma PF, Gao CC, Yi J, et al. Cytotherapy with M1‐polarized macrophages ameliorates liver fibrosis by modulating immune microenvironment in mice. J Hepatol. 2017;67(4):770‐779.
Not in our library10.1016/j.jhep.2017.05.022
- 61.
Ishikawa S, Noma T, Fu HY, et al. Apoptosis inhibitor of macrophage depletion decreased M1 macrophage accumulation and the incidence of cardiac rupture after myocardial infarction in mice. PLoS One. 2017;12(11):e0187894.
Not in our library10.1371/journal.pone.0187894
- 62.
Louiselle AE, Niemiec SM, Zgheib C, Liechty KW. Macrophage polarization and diabetic wound healing. Transl Res. 2021;236:109‐116.
Not in our library10.1016/j.trsl.2021.05.006
- 63.
Sharifiaghdam M, Shaabani E, Faridi‐Majidi R, De Smedt SC, Braeckmans K, Fraire JC. Macrophages as a therapeutic target to promote diabetic wound healing. Mol Ther. 2022;30(9):2891‐2908.
Not in our library10.1016/j.ymthe.2022.07.016
- 64.
Gao X, Lu C, Miao Y, Ren J, Cai X. Role of macrophage polarisation in skin wound healing. Int Wound J. 2023;20(7):2551‐2562.
Not in our library10.1111/iwj.14119
- 65.
He Y, Gao Y, Zhang Q, Zhou G, Cao F, Yao S. IL‐4 switches microglia/macrophage M1/M2 polarization and alleviates neurological damage by modulating the JAK1/STAT6 pathway following ICH. Neuroscience. 2020;437:161‐171.
Not in our library10.1016/j.neuroscience.2020.03.008
- 66.
Gao S, Zhou J, Liu N, et al. Curcumin induces M2 macrophage polarization by secretion IL‐4 and/or IL‐13. J Mol Cell Cardiol. 2015;85:131‐139.
Not in our library10.1016/j.yjmcc.2015.04.025
- 67.
Lundahl MLE, Mitermite M, Ryan DG, et al. Macrophage innate training induced by IL‐4 and IL‐13 activation enhances OXPHOS driven anti‐mycobacterial responses. Elife. 2022;11:e74690.
Not in our library10.7554/elife.74690
- 68.
Huang X, Li Y, Fu M, Xin HB. Polarizing Macrophages In Vitro. Methods Mol Biol. 2018;1784:119‐126.
Not in our library10.1007/978-1-4939-7837-3_12
- 69.
Qu R, Zhou M, Qiu Y, et al. Glucocorticoids improve the balance of M1/M2 macrophage polarization in experimental autoimmune uveitis through the P38MAPK‐MEF2C axis. Int Immunopharmacol. 2023;120:110392.
Not in our library10.1016/j.intimp.2023.110392
- 70.
Luo L, Wang S, Hu Y, et al. Precisely Regulating M2 Subtype Macrophages for Renal Fibrosis Resolution. ACS Nano. 2023;17(22):22508‐22526.
Not in our library10.1021/acsnano.3c05998
- 71.
Chen S, Wang M, Lu T, et al. JMJD6 in tumor‐associated macrophage regulates macrophage polarization and cancer progression via STAT3/IL‐10 axis. Oncogene. 2023;42(37):2737‐2750.
Not in our library10.1038/s41388-023-02781-9
- 72.
- 73.
Kiseleva V, Vishnyakova P, Elchaninov A, Fatkhudinov T, Sukhikh G. Biochemical and molecular inducers and modulators of M2 macrophage polarization in clinical perspective. Int Immunopharmacol. 2023;122:110583.
Not in our library10.1016/j.intimp.2023.110583
- 74.
Fang J, Ou Q, Wu B, et al. TcpC inhibits M1 but promotes M2 macrophage polarization via regulation of the MAPK/NF‐κB and Akt/STAT6 pathways in urinary tract infection. Cells. 2022;11(17):2674.
Not in our library10.3390/cells11172674
- 75.
- 76.
- 77.
Zhu Y, Sun X, Tan S, et al. M2 macrophage‐related gene signature in chronic rhinosinusitis with nasal polyps. Front Immunol. 2022;13:1047930.
Not in our library10.3389/fimmu.2022.1047930
- 78.
Mahon OR, Browe DC, Gonzalez‐Fernandez T, et al. Nano‐particle mediated M2 macrophage polarization enhances bone formation and MSC osteogenesis in an IL‐10 dependent manner. Biomaterials. 2020;239:119833.
Not in our library10.1016/j.biomaterials.2020.119833
- 79.
- 80.
- 81.
Fu XH, Li JP, Li XY, et al. M2‐macrophage‐derived exosomes promote meningioma progression through TGF‐β signaling pathway. J Immunol Res. 2022;2022:8326591.
Not in our library10.1155/2022/8326591
- 82.
Cai G, Lu Y, Zhong W, et al. Piezo1‐mediated M2 macrophage mechanotransduction enhances bone formation through secretion and activation of transforming growth factor‐β1. Cell Prolif. 2023;56(9):e13440.
Not in our library10.1111/cpr.13440
- 83.
- 84.
Oh S, Lee JH, Kim HM, et al. Poly‐L‐lactic acid fillers improved dermal collagen synthesis by modulating M2 macrophage polarization in aged animal skin. Cells. 2023;12(9):1320.
Not in our library10.3390/cells12091320
- 85.
Li S, Ding X, Zhang H, Ding Y, Tan Q. IL‐25 improves diabetic wound healing through stimulating M2 macrophage polarization and fibroblast activation. Int Immunopharmacol. 2022;106:108605.
Not in our library10.1016/j.intimp.2022.108605
- 86.
Wang Y, Geng X, Guo Z, et al. M2 macrophages promote subconjunctival fibrosis through YAP/TAZ signalling. Ann Med. 2024;56(1):2313680.
Not in our library10.1080/07853890.2024.2313680
- 87.
Zhang J, Muri J, Fitzgerald G, et al. Endothelial lactate controls muscle regeneration from ischemia by inducing M2‐like macrophage polarization. Cell Metab. 2020;31(6):1136‐1153. e7.
Not in our library10.1016/j.cmet.2020.05.004
- 88.
- 89.
Xu H, Zhu Y, Hsiao AW, et al. Bioactive glass‐elicited stem cell‐derived extracellular vesicles regulate M2 macrophage polarization and angiogenesis to improve tendon regeneration and functional recovery. Biomaterials. 2023;294:121998.
Not in our library10.1016/j.biomaterials.2023.121998
- 90.
Razi S, Yaghmoorian Khojini J, Kargarijam F, et al. Macrophage efferocytosis in health and disease. Cell Biochem Funct. 2023;41(2):152‐165.
Not in our library10.1002/cbf.3780
- 91.
- 92.
Zhong X, Lee HN, Kim SH, et al. Myc‐nick promotes efferocytosis through M2 macrophage polarization during resolution of inflammation. Faseb J. 2018;32(10):5312‐5325.
Not in our library10.1096/fj.201800223r
- 93.
Govindappa PK, Elfar JC. Erythropoietin promotes M2 macrophage phagocytosis of Schwann cells in peripheral nerve injury. Cell Death Dis. 2022;13(3):245.
Not in our library10.1038/s41419-022-04671-6
- 94.
Ying W, Gao H, Dos Reis FCG, et al. MiR‐690, an exosomal‐derived miRNA from M2‐polarized macrophages, improves insulin sensitivity in obese mice. Cell Metab. 2021;33(4):781‐790. e5.
Not in our library10.1016/j.cmet.2020.12.019
- 95.
- 96.
- 97.
Savitri C, Kwon JW, Drobyshava V, Ha SS, Park K. M2 macrophage‐derived concentrated conditioned media significantly improves skin wound healing. Tissue Eng Regen Med. 2022;19(3):617‐628.
Not in our library10.1007/s13770-021-00414-4
- 98.
- 99.
Li S, Yang P, Ding X, Zhang H, Ding Y, Tan Q. Puerarin improves diabetic wound healing via regulation of macrophage M2 polarization phenotype. Burns Trauma. 2022;10:tkac046.
Not in our library10.1093/burnst/tkac046
- 100.
Anders CB, Lawton TMW, Ammons MCB. Metabolic immunomodulation of macrophage functional plasticity in nonhealing wounds. Curr Opin Infect Dis. 2019;32(3):204‐209.
Not in our library10.1097/qco.0000000000000550
- 101.
Hourani T, Perez‐Gonzalez A, Khoshmanesh K, et al. Label‐free macrophage phenotype classification using machine learning methods. Sci Rep. 2023;13(1):5202.
Not in our library10.1038/s41598-023-32158-7
- 102.
Ordaz‐Arias MA, Díaz‐Alvarez L, Zúñiga J, Martinez‐Sánchez ME, Balderas‐Martínez YI. Cyclic attractors are critical for macrophage differentiation, heterogeneity, and plasticity. Front Mol Biosci. 2022;9:807228.
Not in our library10.3389/fmolb.2022.807228
- 103.
- 104.
Nakai K. Multiple roles of macrophage in skin. J Dermatol Sci. 2021;104(1):2‐10.
Not in our library10.1016/j.jdermsci.2021.08.008
- 105.
Anders CB, Lawton TMW, Smith HL, Garret J, Doucette MM, Ammons MCB. Use of integrated metabolomics, transcriptomics, and signal protein profile to characterize the effector function and associated metabotype of polarized macrophage phenotypes. J Leukoc Biol. 2022;111(3):667‐693.
Not in our library10.1002/jlb.6a1120-744r
- 106.
Kang H, Bang JY, Mo Y, et al. Effect of Acinetobacter lwoffii on the modulation of macrophage activation and asthmatic inflammation. Clin Exp Allergy. 2022;52(4):518‐529.
Not in our library10.1111/cea.14077
- 107.
Kuo CH, Tsai ML, Li CH, et al. Altered pattern of macrophage polarization as a biomarker for severity of childhood asthma. J Inflamm Res. 2021;14:6011‐6023.
Not in our library10.2147/jir.s319754
- 108.
Feng D, Huang WY, Niu XL, Hao S, Zhang LN, Hu YJ. Significance of macrophage subtypes in the peripheral blood of children with systemic juvenile idiopathic arthritis. Rheumatol Ther. 2021;8(4):1859‐1870.
Not in our library10.1007/s40744-021-00385-x
- 109.
Fan P, Zhang Y, Ding S, Du Z, Zhou C, Du X. Integrating RNA‐seq and scRNA‐seq to explore the mechanism of macrophage ferroptosis associated with COPD. Front Pharmacol. 2023;14:1139137.
Not in our library10.3389/fphar.2023.1139137
- 110.
Barreby E, Chen P, Aouadi M. Macrophage functional diversity in NAFLD ‐ more than inflammation. Nat Rev Endocrinol. 2022;18(8):461‐472.
Not in our library10.1038/s41574-022-00675-6
- 111.
- 112.
Ransohoff RM. A polarizing question: do M1 and M2 microglia exist? Nat Neurosci. 2016;19(8):987‐991.
Not in our library10.1038/nn.4338
- 113.
Angel CE, Chen CJJ, Horlacher OC, et al. Distinctive localization of antigen‐presenting cells in human lymph nodes. Immunobiology. 2009;113(6):1257‐1267
Not in our library10.1182/blood-2008-06-165266
- 114.
Aegerter H, Lambrecht BN, Jakubzick CV. Biology of lung macrophages in health and disease. Immunity. 2022;55(9):1564‐1580.
Not in our library10.1016/j.immuni.2022.08.010
- 115.
Yao C, Cao Y, Wang D, et al. Single‐cell sequencing reveals microglia induced angiogenesis by specific subsets of endothelial cells following spinal cord injury. Faseb J. 2022;36(7):e22393.
Not in our library10.1096/fj.202200337r
- 116.
Yue Z, Nie L, Zhang P, Chen Q, Lv Q, Wang Q. Tissue‐resident macrophage inflammaging aggravates homeostasis dysregulation in age‐related diseases. Cell Immunol. 2021;361:104278.
Not in our library10.1016/j.cellimm.2020.104278
- 117.
Gosselin D, Link VM, Romanoski CE, et al. Environment drives selection and function of enhancers controlling tissue‐specific macrophage identities. Cell. 2014;159(6):1327‐1340.
Not in our library10.1016/j.cell.2014.11.023
- 118.
Blériot C, Chakarov S, Ginhoux F. Determinants of resident tissue macrophage identity and function. Immunity. 2020;52(6):957‐970.
Not in our library10.1016/j.immuni.2020.05.014
- 119.
Delfini M, Stakenborg N, Viola MF, Boeckxstaens G. Macrophages in the gut: masters in multitasking. Immunity. 2022;55(9):1530‐1548.
Not in our library10.1016/j.immuni.2022.08.005
- 120.
Gabanyi I, Muller PA, Feighery L, Oliveira TY, Costa‐Pinto FA, Mucida D. Neuro‐immune interactions drive tissue programming in intestinal macrophages. Cell. 2016;164(3):378‐391.
Not in our library10.1016/j.cell.2015.12.023
- 121.
- 122.
Duan H, Wang L, Huangfu M, Li H. The impact of microbiota‐derived short‐chain fatty acids on macrophage activities in disease: mechanisms and therapeutic potentials. Biomed Pharmacother. 2023;165:115276.
Not in our library10.1016/j.biopha.2023.115276
- 123.
Meng L, Lu C, Wu B, et al. Taurine antagonizes macrophages M1 polarization by mitophagy‐glycolysis switch blockage via dragging SAM‐PP2Ac transmethylation. Front Immunol. 2021;12:648913.
Not in our library10.3389/fimmu.2021.648913
- 124.
Jia D, Chen S, Bai P, et al. Cardiac resident macrophage‐derived legumain improves cardiac repair by promoting clearance and degradation of apoptotic cardiomyocytes after myocardial infarction. Circulation. 2022;145(20):1542‐1556.
Not in our library10.1161/circulationaha.121.057549
- 125.
Hill DA, Lim HW, Kim YH, et al. Distinct macrophage populations direct inflammatory versus physiological changes in adipose tissue. Proc Natl Acad Sci USA. 2018;115(22):E5096‐E5105.
Not in our library10.1073/pnas.1802611115
- 126.
Lazarov T, Juarez‐Carreño S, Cox N, Geissmann F. Physiology and diseases of tissue‐resident macrophages. Nature. 2023;618(7966):698‐707.
Not in our library10.1038/s41586-023-06002-x
- 127.
- 128.
Yona S, Kim KW, Wolf Y, et al. Fate mapping reveals origins and dynamics of monocytes and tissue macrophages under homeostasis. Immunity. 2013;38(1):79‐91.
Not in our library10.1016/j.immuni.2012.12.001
- 129.
Xu Y, Schrank PR, Williams JW. Macrophage fate mapping. Curr Protoc. 2022;2(6):e456.
Not in our library10.1002/cpz1.456
- 130.
Prinz M, Masuda T, Wheeler MA, Quintana FJ. Microglia and central nervous system‐associated macrophages‐from origin to disease modulation. Annu Rev Immunol. 2021;39:251‐277.
Not in our library10.1146/annurev-immunol-093019-110159
- 131.
Fan X, Lu P, Cui XH, et al. Repopulating Kupffer cells originate directly from hematopoietic stem cells. Stem Cell Res Ther. 2023;14(1):351.
Not in our library10.1186/s13287-023-03569-0
- 132.
Dick SA, Wong A, Hamidzada H, et al. Three tissue resident macrophage subsets coexist across organs with conserved origins and life cycles. Sci Immunol. 2022;7(67):eabf7777.
Not in our library10.1126/sciimmunol.abf7777
- 133.
Richoz N, Tuong ZK, Loudon KW, et al. Distinct pathogenic roles for resident and monocyte‐derived macrophages in lupus nephritis. JCI Insight. 2022;7(21):e159751.
Not in our library10.1172/jci.insight.159751
- 134.
Rizzo G, Gropper J, Piollet M, et al. Dynamics of monocyte‐derived macrophage diversity in experimental myocardial infarction. Cardiovasc Res. 2023;119(3):772‐785.
Not in our library10.1093/cvr/cvac113
- 135.
Kloc M, Kubiak JZ. Monocyte and macrophage function diversity. Int J Mol Sci. 2022;23(20):12404.
Not in our library10.3390/ijms232012404
- 136.
Ochando J, Mulder WJM, Madsen JC, Netea MG, Duivenvoorden R. Trained immunity ‐ basic concepts and contributions to immunopathology. Nat Rev Nephrol. 2023;19(1):23‐37.
Not in our library10.1038/s41581-022-00633-5
- 137.
Guo Z, Wang L, Liu H, Xie Y. Innate immune memory in monocytes and macrophages: the potential therapeutic strategies for atherosclerosis. Cells. 2022;11(24):4072.
Not in our library10.3390/cells11244072
- 138.
Ferluga J, Yasmin H, Al‐Ahdal MN, Bhakta S, Kishore U. Natural and trained innate immunity against Mycobacterium tuberculosis. Immunobiology. 2020;225(3):151951.
Not in our library10.1016/j.imbio.2020.151951
- 139.
- 140.
Arts RJ, Blok BA, van Crevel R, et al. Vitamin A induces inhibitory histone methylation modifications and down‐regulates trained immunity in human monocytes. J Leukoc Biol. 2015;98(1):129‐136.
Not in our library10.1189/jlb.6ab0914-416r
- 141.
Adams K, Weber KS, Johnson SM. Exposome and immunity training: how pathogen exposure order influences innate immune cell lineage commitment and function. Int J Mol Sci. 2020;21(22):8462.
Not in our library10.3390/ijms21228462
- 142.
- 143.
Mora VP, Loaiza RA, Soto JA, Bohmwald K, Kalergis AM. Involvement of trained immunity during autoimmune responses. J Autoimmun. 2023;137:102956.
Not in our library10.1016/j.jaut.2022.102956
- 144.
Fani Maleki A, Cisbani G, Plante MM, et al. Muramyl dipeptide‐mediated immunomodulation on monocyte subsets exerts therapeutic effects in a mouse model of Alzheimer's disease. J Neuroinflammation. 2020;17(1):218.
Not in our library10.1186/s12974-020-01893-3
- 145.
Moorlag S, Rodriguez‐Rosales YA, Gillard J, et al. BCG vaccination induces long‐term functional reprogramming of human neutrophils. Cell Rep. 2020;33(7):108387.
Not in our library10.1016/j.celrep.2020.108387
- 146.
Vázquez‐Carballo C, Guerrero‐Hue M, García‐Caballero C, et al. Toll‐like receptors in acute kidney injury. Int J Mol Sci. 2021;22(2):816.
Not in our library10.3390/ijms22020816
- 147.
- 148.
Onyishi CU, Desanti GE, Wilkinson AL, et al. Toll‐like receptor 4 and macrophage scavenger receptor 1 crosstalk regulates phagocytosis of a fungal pathogen. Nat Commun. 2023;14(1):4895.
Not in our library10.1038/s41467-023-40635-w
- 149.
Kirchner S, Lei V, MacLeod AS. The cutaneous wound innate immunological microenvironment. Int J Mol Sci. 2020;21(22):8748.
Not in our library10.3390/ijms21228748
- 150.
Wang L, Wang J, Han L, Chen T. Palmatine attenuated lipopolysaccharide‐induced acute lung injury by inhibiting M1 phenotype macrophage polarization via NAMPT/TLR2/CCR1 signaling. J Agric Food Chem. 2024.
Not in our library10.1021/acs.jafc.3c05597
- 151.
Owen AM, Luan L, Burelbach KR, et al. MyD88‐dependent signaling drives toll‐like receptor‐induced trained immunity in macrophages. Front Immunol. 2022;13:1044662.
Not in our library10.3389/fimmu.2022.1044662
- 152.
Hsieh WY, Zhou QD, York AG, et al. Toll‐like receptors induce signal‐specific reprogramming of the macrophage lipidome. Cell Metab. 2020;32(1):128‐143. e5.
Not in our library10.1016/j.cmet.2020.05.003
- 153.
Yamamoto M, Sato S, Hemmi H, et al. Role of adaptor TRIF in the MyD88‐independent toll‐like receptor signaling pathway. Science. 2003;301(5633):640‐643.
Not in our library10.1126/science.1087262
- 154.
Pereira M, Durso DF, Bryant CE, et al. The IRAK4 scaffold integrates TLR4‐driven TRIF and MYD88 signaling pathways. Cell Rep. 2022;40(7):111225.
Not in our library10.1016/j.celrep.2022.111225
- 155.
Luo X, Bao X, Weng X, et al. The protective effect of quercetin on macrophage pyroptosis via TLR2/Myd88/NF‐κB and ROS/AMPK pathway. Life Sci. 2022;291:120064.
Not in our library10.1016/j.lfs.2021.120064
- 156.
Li Y, Zhang L, Ren P, et al. Qing‐Xue‐Xiao‐Zhi formula attenuates atherosclerosis by inhibiting macrophage lipid accumulation and inflammatory response via TLR4/MyD88/NF‐κB pathway regulation. Phytomedicine. 2021;93:153812.
Not in our library10.1016/j.phymed.2021.153812
- 157.
McKiel LA, Woodhouse KA, Fitzpatrick LE. A macrophage reporter cell assay to examine toll‐like receptor‐mediated NF‐kB/AP‐1 signaling on adsorbed protein layers on polymeric surfaces. J Vis Exp. 2020;(155):
Not in our library10.3791/60317
- 158.
Hannemann N, Cao S, Eriksson D, et al. Transcription factor Fra‐1 targets arginase‐1 to enhance macrophage‐mediated inflammation in arthritis. J Clin Invest. 2019;129(7):2669‐2684.
Not in our library10.1172/jci96832
- 159.
Negishi H, Ohba Y, Yanai H, et al. Negative regulation of Toll‐like‐receptor signaling by IRF‐4. Proc Natl Acad Sci USA. 2005;102(44):15989‐15994.
Not in our library10.1073/pnas.0508327102
- 160.
Wu L, Chen L, Li H, et al. Nocardia rubra cell‐wall skeleton mitigates whole abdominal irradiation‐induced intestinal injury via regulating macrophage function. Burns Trauma. 2024;12:tkad045.
Not in our library10.1093/burnst/tkad045
- 161.
Olona A, Hateley C, Muralidharan S, Wenk MR, Torta F, Behmoaras J. Sphingolipid metabolism during Toll‐like receptor 4 (TLR4)‐mediated macrophage activation. Br J Pharmacol. 2021;178(23):4575‐4587.
Not in our library10.1111/bph.15642
- 162.
Ye Y, Wang Y, Yang Y, Tao L. Aloperine suppresses LPS‐induced macrophage activation through inhibiting the TLR4/NF‐κB pathway. Inflamm Res. 2020;69(4):375‐383.
Not in our library10.1007/s00011-019-01313-0
- 163.
Zhang Y, Song Y, Du J, et al. S100 calcium‐binding protein A9 promotes skin regeneration through toll‐like receptor 4 during tissue expansion. Burns Trauma. 2023;11:tkad030.
Not in our library10.1093/burnst/tkad030
- 164.
Xie XD, Tang M, Yi SL, et al. Polysaccharide of Asparagus cochinchinensis (Lour.) Merr regulates macrophage immune response and epigenetic memory through TLR4‐JNK/p38/ERK signaling pathway and histone modification. Phytomedicine. 2024;124:155294.
Not in our library10.1016/j.phymed.2023.155294
- 165.
Bode JG, Ehlting C, Häussinger D. The macrophage response towards LPS and its control through the p38(MAPK)‐STAT3 axis. Cell Signal. 2012;24(6):1185‐1194.
Not in our library10.1016/j.cellsig.2012.01.018
- 166.
Hu J, Wang H, Li X, et al. Fibrinogen‐like protein 2 aggravates nonalcoholic steatohepatitis via interaction with TLR4, eliciting inflammation in macrophages and inducing hepatic lipid metabolism disorder. Theranostics. 2020;10(21):9702‐9720.
Not in our library10.7150/thno.44297
- 167.
Xiao J, Li W, Zheng X, et al. Targeting 7‐dehydrocholesterol reductase integrates cholesterol metabolism and IRF3 activation to eliminate infection. Immunity. 2020;52(1):109‐122. e6.
Not in our library10.1016/j.immuni.2019.11.015
- 168.
Seebach E, Sonnenmoser G, Kubatzky KF. Staphylococcus aureus planktonic but not biofilm environment induces an IFN‐β macrophage immune response via the STING/IRF3 pathway. Virulence. 2023;14(1):2254599.
Not in our library10.1080/21505594.2023.2254599
- 169.
Zhang C, Cheng N, Qiao B, et al. Age‐related decline of interferon‐gamma responses in macrophage impairs satellite cell proliferation and regeneration. J Cachexia Sarcopenia Muscle. 2020;11(5):1291‐1305.
Not in our library10.1002/jcsm.12584
- 170.
Zheng M, Karki R, Williams EP, et al. TLR2 senses the SARS‐CoV‐2 envelope protein to produce inflammatory cytokines. Nat Immunol. 2021;22(7):829‐838.
Not in our library10.1038/s41590-021-00937-x
- 171.
- 172.
Qian Y, Chu G, Zhang L, et al. M2 macrophage‐derived exosomal miR‐26b‐5p regulates macrophage polarization and chondrocyte hypertrophy by targeting TLR3 and COL10A1 to alleviate osteoarthritis. J Nanobiotechnology. 2024;22(1):72.
Not in our library10.1186/s12951-024-02336-4
- 173.
Gundra UM, Mishra BB, Wong K, Teale JM. Increased disease severity of parasite‐infected TLR2‐/‐ mice is correlated with decreased central nervous system inflammation and reduced numbers of cells with alternatively activated macrophage phenotypes in a murine model of neurocysticercosis. Infect Immun. 2011;79(7):2586‐2596.
Not in our library10.1128/iai.00920-10
- 174.
Li W, Wang K, Liu Y, et al. A novel drug combination of mangiferin and cinnamic acid alleviates rheumatoid arthritis by inhibiting TLR4/NFκB/NLRP3 activation‐induced pyroptosis. Front Immunol. 2022;13:912933.
Not in our library10.3389/fimmu.2022.912933
- 175.
Li L, Pan Z, Ning D, Fu Y. Rosmanol and carnosol synergistically alleviate rheumatoid arthritis through inhibiting TLR4/NF‐κB/MAPK pathway. Molecules. 2021;27(1):78.
Not in our library10.3390/molecules27010078
- 176.
Dai W, Long L, Wang X, Li S, Xu H. Phytochemicals targeting Toll‐like receptors 4 (TLR4) in inflammatory bowel disease. Chin Med. 2022;17(1):53.
Not in our library10.1186/s13020-022-00611-w
- 177.
Liu B, Wang X, Chen TZ, et al. Polarization of M1 tumor associated macrophage promoted by the activation of TLR3 signal pathway. Asian Pac J Trop Med. 2016;9(5):484‐488.
Not in our library10.1016/j.apjtm.2016.03.019
- 178.
Thomas G, Micci L, Yang W, et al. Intra‐tumoral activation of endosomal TLR pathways reveals a distinct role for TLR3 agonist dependent type‐1 interferons in shaping the tumor immune microenvironment. Front Oncol. 2021;11:711673.
Not in our library10.3389/fonc.2021.711673
- 179.
Zhou D, Huang C, Lin Z, et al. Macrophage polarization and function with emphasis on the evolving roles of coordinated regulation of cellular signaling pathways. Cell Signal. 2014;26(2):192‐197.
Not in our library10.1016/j.cellsig.2013.11.004
- 180.
Li L, Wei C, Cai S, Fang L. TRPM7 modulates macrophage polarization by STAT1/STAT6 pathways in RAW264.7 cells. Biochem Biophys Res Commun. 2020;533(4):692‐697.
Not in our library10.1016/j.bbrc.2020.10.062
- 181.
Liu Y, Liu Z, Tang H, et al. The N(6)‐methyladenosine (m(6)A)‐forming enzyme METTL3 facilitates M1 macrophage polarization through the methylation of STAT1 mRNA. Am J Physiol Cell Physiol. 2019;317(4):C762‐C775.
Not in our library10.1152/ajpcell.00212.2019
- 182.
Jerke U, Tkachuk S, Kiyan J, et al. Stat1 nuclear translocation by nucleolin upon monocyte differentiation. PLoS One. 2009;4(12):e8302.
Not in our library10.1371/journal.pone.0008302
- 183.
Chattopadhyay D, Das S, Guria S, Basu S, Mukherjee S. Fetuin‐A regulates adipose tissue macrophage content and activation in insulin resistant mice through MCP‐1 and iNOS: involvement of IFNγ‐JAK2‐STAT1 pathway. Biochem J. 2021;478(22):4027‐4043.
Not in our library10.1042/bcj20210442
- 184.
Yang T, Wang R, Liu H, et al. Berberine regulates macrophage polarization through IL‐4‐STAT6 signaling pathway in Helicobacter pylori‐induced chronic atrophic gastritis. Life Sci. 2021;266:118903.
Not in our library10.1016/j.lfs.2020.118903
- 185.
Shi JH, Liu LN, Song DD, et al. TRAF3/STAT6 axis regulates macrophage polarization and tumor progression. Cell Death Differ. 2023;30(8):2005‐2016.
Not in our library10.1038/s41418-023-01194-1
- 186.
- 187.
Rahal OM, Wolfe AR, Mandal PK, et al. Blocking interleukin (IL)4‐ and IL13‐mediated phosphorylation of STAT6 (Tyr641) decreases M2 polarization of macrophages and protects against macrophage‐mediated radioresistance of inflammatory breast cancer. Int J Radiat Oncol Biol Phys. 2018;100(4):1034‐1043.
Not in our library10.1016/j.ijrobp.2017.11.043
- 188.
Xiang X, Feng D, Hwang S, et al. Interleukin‐22 ameliorates acute‐on‐chronic liver failure by reprogramming impaired regeneration pathways in mice. J Hepatol. 2020;72(4):736‐745.
Not in our library10.1016/j.jhep.2019.11.013
- 189.
Sun W, Wang Q, Zhang R, Zhang N. Ketogenic diet attenuates neuroinflammation and induces conversion of M1 microglia to M2 in an EAE model of multiple sclerosis by regulating the NF‐κB/NLRP3 pathway and inhibiting HDAC3 and P2×7R activation. Food Funct. 2023;14(15):7247‐7269.
Not in our library10.1039/d3fo00122a
- 190.
Covarrubias AJ, Aksoylar HI, Horng T. Control of macrophage metabolism and activation by mTOR and Akt signaling. Semin Immunol. 2015;27(4):286‐296.
Not in our library10.1016/j.smim.2015.08.001
- 191.
Donninelli G, Saraf‐Sinik I, Mazziotti V, et al. Interleukin‐9 regulates macrophage activation in the progressive multiple sclerosis brain. J Neuroinflammation. 2020;17(1):149.
Not in our library10.1186/s12974-020-01770-z
- 192.
Geng T, Yan Y, Xu L, et al. CD137 signaling induces macrophage M2 polarization in atherosclerosis through STAT6/PPARδ pathway. Cell Signal. 2020;72:109628.
Not in our library10.1016/j.cellsig.2020.109628
- 193.
Gong M, Zhuo X, Ma A. STAT6 upregulation promotes M2 macrophage polarization to suppress atherosclerosis. Med Sci Monit Basic Res. 2017;23:240‐249.
Not in our library10.12659/msmbr.904014
- 194.
Czimmerer Z, Nagy L. Epigenomic regulation of macrophage polarization: Where do the nuclear receptors belong? Immunol Rev. 2023;317(1):152‐165.
Not in our library10.1111/imr.13209
- 195.
Tu Y, Liu J, Kong D, et al. Irisin drives macrophage anti‐inflammatory differentiation via JAK2‐STAT6‐dependent activation of PPARγ and Nrf2 signaling. Free Radic Biol Med. 2023;201:98‐110.
Not in our library10.1016/j.freeradbiomed.2023.03.014
- 196.
Sharma S, Shen T, Chitranshi N, et al. Retinoid X receptor: cellular and biochemical roles of nuclear receptor with a focus on neuropathological involvement. Mol Neurobiol. 2022;59(4):2027‐2050.
Not in our library10.1007/s12035-021-02709-y
- 197.
He L, Jhong JH, Chen Q, et al. Global characterization of macrophage polarization mechanisms and identification of M2‐type polarization inhibitors. Cell Rep. 2021;37(5):109955.
Not in our library10.1016/j.celrep.2021.109955
- 198.
Yu T, Gao M, Yang P, et al. Insulin promotes macrophage phenotype transition through PI3K/Akt and PPAR‐γ signaling during diabetic wound healing. J Cell Physiol. 2019;234(4):4217‐4231.
Not in our library10.1002/jcp.27185
- 199.
Xu M, Wang X, Li Y, et al. Arachidonic acid metabolism controls macrophage alternative activation through regulating oxidative phosphorylation in PPARγ dependent manner. Front Immunol. 2021;12:618501.
Not in our library10.3389/fimmu.2021.618501
- 200.
Ding H, Dong J, Wang Y, et al. Ginsenoside Rb1 interfered with macrophage activation by activating PPARγ to inhibit insulin resistance in obesity. Molecules. 2023;28(7):3083.
Not in our library10.3390/molecules28073083
- 201.
de la Aleja AG, Herrero C, Torres‐Torresano M, et al. Inhibition of LXR controls the polarization of human inflammatory macrophages through upregulation of MAFB. Cell Mol Life Sci. 2023;80(4):96.
Not in our library10.1007/s00018-023-04745-4
- 202.
Dong XC. Sirtuin 6—a key regulator of hepatic lipid metabolism and liver health. Cells. 2023;12(4):663.
Not in our library10.3390/cells12040663
- 203.
Zhang X, McDonald JG, Aryal B, et al. Desmosterol suppresses macrophage inflammasome activation and protects against vascular inflammation and atherosclerosis. Proc Natl Acad Sci USA. 2021;118(47):e2107682118.
Not in our library10.1073/pnas.2107682118
- 204.
Li X, Huang X, Feng Y, et al. Cylindrin from Imperata cylindrica inhibits M2 macrophage formation and attenuates renal fibrosis by downregulating the LXR‐α/PI3K/AKT pathway. Eur J Pharmacol. 2023;950:175771.
Not in our library10.1016/j.ejphar.2023.175771
- 205.
Oishi Y, Spann NJ, Link VM, et al. SREBP1 contributes to resolution of pro‐inflammatory TLR4 signaling by reprogramming fatty acid metabolism. Cell Metab. 2017;25(2):412‐427.
Not in our library10.1016/j.cmet.2016.11.009
- 206.
Chuang ST, Stein JB, Nevins S, et al. Enhancing CAR macrophage efferocytosis via surface engineered lipid nanoparticles targeting LXR signaling. Adv Mater. 2024;36(19):e2308377.
Not in our library10.1002/adma.202308377
- 207.
Babuta M, Szabo G. Extracellular vesicles in inflammation: focus on the microRNA cargo of EVs in modulation of liver diseases. J Leukoc Biol. 2022;111(1):75‐92.
Not in our library10.1002/jlb.3mir0321-156r
- 208.
Nandan D, Rath CT, Reiner NE. Leishmania regulates host macrophage miRNAs expression by engaging transcription factor c‐Myc. J Leukoc Biol. 2021;109(5):999‐1007.
Not in our library10.1002/jlb.4ru0920-614r
- 209.
Yang B, Lin Y, Huang Y, Zhu N, Shen Y‐Q. Extracellular vesicles modulate key signalling pathways in refractory wound healing. Burns Trauma. 2023;11:tkad039.
Not in our library10.1093/burnst/tkad039
- 210.
Ye J, Kang Y, Sun X, Ni P, Wu M, Lu S. MicroRNA‐155 inhibition promoted wound healing in diabetic rats. Int J Low Extrem Wounds. 2017;16(2):74‐84.
Not in our library10.1177/1534734617706636
- 211.
Chachques JC, Gardin C, Lila N, et al. Elastomeric cardiowrap scaffolds functionalized with mesenchymal stem cells‐derived exosomes induce a positive modulation in the inflammatory and wound healing response of mesenchymal stem cell and macrophage. Biomedicines. 2021;9(7):824.
Not in our library10.3390/biomedicines9070824
- 212.
Zheng L, Su J, Zhang Z, et al. Salidroside regulates inflammatory pathway of alveolar macrophages by influencing the secretion of miRNA‐146a exosomes by lung epithelial cells. Sci Rep. 2020;10(1):20750.
Not in our library10.1038/s41598-020-77448-6
- 213.
Bala S, Csak T, Saha B, et al. The pro‐inflammatory effects of miR‐155 promote liver fibrosis and alcohol‐induced steatohepatitis. J Hepatol. 2016;64(6):1378‐1387.
Not in our library10.1016/j.jhep.2016.01.035
- 214.
Gao Y, Han T, Han C, et al. Propofol regulates the TLR4/NF‐κB pathway through miRNA‐155 to protect colorectal cancer intestinal barrier. Inflammation. 2021;44(5):2078‐2090.
Not in our library10.1007/s10753-021-01485-0
- 215.
Chaudhuri AA, So AY, Sinha N, et al. MicroRNA‐125b potentiates macrophage activation. J Immunol. 2011;187(10):5062‐5068.
Not in our library10.4049/jimmunol.1102001
- 216.
Peng X, He F, Mao Y, et al. miR‐146a promotes M2 macrophage polarization and accelerates diabetic wound healing by inhibiting the TLR4/NF‐κB axis. J Mol Endocrinol. 2022;69(2):315‐327.
Not in our library10.1530/jme-21-0019
- 217.
- 218.
Ponomarev ED, Veremeyko T, Barteneva N, Krichevsky AM, Weiner HL. MicroRNA‐124 promotes microglia quiescence and suppresses EAE by deactivating macrophages via the C/EBP‐α‐PU.1 pathway. Nat Med. 2011;17(1):64‐70.
Not in our library10.1038/nm.2266
- 219.
Ding N, Luo G, Li H, et al. A cyclodextrin‐based ph‐responsive microRNA delivery platform targeting polarization of M1 to M2 macrophages for sepsis therapy. Adv Healthc Mater. 2023;12(27):e2301243.
Not in our library10.1002/adhm.202301243
- 220.
Ying W, Tseng A, Chang RC, et al. MicroRNA‐223 is a crucial mediator of PPARγ‐regulated alternative macrophage activation. J Clin Invest. 2015;125(11):4149‐4159.
Not in our library10.1172/jci81656
- 221.
Amoruso A, Blonda M, Gironi M, et al. Immune and central nervous system‐related miRNAs expression profiling in monocytes of multiple sclerosis patients. Sci Rep. 2020;10(1):6125.
Not in our library10.1038/s41598-020-63282-3
- 222.
Paoletti A, Ly B, Cailleau C, et al. Liposomal AntagomiR‐155‐5p restores anti‐inflammatory macrophages and improves arthritis in preclinical models of rheumatoid arthritis. Arthritis Rheumatol. 2024;76(1):18‐31.
Not in our library10.1002/art.42665
- 223.
Li ZL, Yang BC, Gao M, Xiao XF, Zhao SP, Liu ZL. Naringin improves sepsis‐induced intestinal injury by modulating macrophage polarization via PPARγ/miR‐21 axis. Mol Ther Nucleic Acids. 2021;25:502‐514.
Not in our library10.1016/j.omtn.2021.07.005
- 224.
- 225.
Wang Z, Zhao F, Xu C, et al. Metabolic reprogramming in skin wound healing. Burns Trauma. 2024;12:tkad047.
Not in our library10.1093/burnst/tkad047
- 226.
Mouton AJ, Li X, Hall ME, Hall JE. Obesity, hypertension, and cardiac dysfunction: novel roles of immunometabolism in macrophage activation and inflammation. Circ Res. 2020;126(6):789‐806.
Not in our library10.1161/circresaha.119.312321
- 227.
Wang F, Zhang S, Vuckovic I, et al. Glycolytic stimulation is not a requirement for M2 macrophage differentiation. Cell Metab. 2018;28(3):463‐475. e4.
Not in our library10.1016/j.cmet.2018.08.012
- 228.
Liu T, Wen Z, Shao L, et al. ATF4 knockdown in macrophage impairs glycolysis and mediates immune tolerance by targeting HK2 and HIF‐1α ubiquitination in sepsis. Clin Immunol. 2023;254:109698.
Not in our library10.1016/j.clim.2023.109698
- 229.
- 230.
Tian S, Tan S, Fan M, et al. Hypoxic environment of wounds and photosynthesis‐based oxygen therapy. Burns Trauma. 2024;12:tkae012.
Not in our library10.1093/burnst/tkae012
- 231.
Jin L, Zhou S, Zhao S, et al. Early short‐term hypoxia promotes epidermal cell migration by activating the CCL2‐ERK1/2 pathway and epithelial–mesenchymal transition during wound healing. Burns Trauma. 2024;12:tkae017.
Not in our library10.1093/burnst/tkae017
- 232.
Nascimento Júnior JXD, Sola‐Penna M, Zancan P. Clotrimazole reverses macrophage M2 polarization by disrupting the PI3K/AKT/mTOR pathway. Biochem Biophys Res Commun. 2024;696:149455.
Not in our library10.1016/j.bbrc.2023.149455
- 233.
- 234.
Cheng JW, Yu Y, Zong SY, et al. Berberine ameliorates collagen‐induced arthritis in mice by restoring macrophage polarization via AMPK/mTORC1 pathway switching glycolytic reprogramming. Int Immunopharmacol. 2023;124(Pt B):111024.
Not in our library10.1016/j.intimp.2023.111024
- 235.
Yang Y, Wang J, Guo S, et al. Non‐lethal sonodynamic therapy facilitates the M1‐to‐M2 transition in advanced atherosclerotic plaques via activating the ROS‐AMPK‐mTORC1‐autophagy pathway. Redox Biol. 2020;32:101501.
Not in our library10.1016/j.redox.2020.101501
- 236.
- 237.
Kim YS, Park BS, Baek HS, Kang HM, Oh JM, Kim IR. Metformin activates AMPK and mTOR to Inhibit RANKL‐stimulated osteoclast formation. Eur Rev Med Pharmacol Sci. 2023;27(18):8795‐8811.
Not in our library10.26355/eurrev_202309_33801
- 238.
- 239.
Xiao S, Qi M, Zhou Q, et al. Macrophage fatty acid oxidation in atherosclerosis. Biomed Pharmacother. 2024;170:116092.
Not in our library10.1016/j.biopha.2023.116092
- 240.
Chang L, Gao J, Yu Y, et al. MMP10 alleviates non‐alcoholic steatohepatitis by regulating macrophage M2 polarization. Int Immunopharmacol. 2023;124(Pt B):111045.
Not in our library10.1016/j.intimp.2023.111045
- 241.
Chen X, He Y, Fu W, et al. Histone deacetylases (HDACs) and atherosclerosis: a mechanistic and pharmacological review. Front Cell Dev Biol. 2020;8:581015.
Not in our library10.3389/fcell.2020.581015
- 242.
Das Gupta K, Shakespear MR, Iyer A, Fairlie DP, Sweet MJ. Histone deacetylases in monocyte/macrophage development, activation and metabolism: refining HDAC targets for inflammatory and infectious diseases. Clin Transl Immunol. 2016;5(1):e62.
Not in our library10.1038/cti.2015.46
- 243.
Karnam K, Sedmaki K, Sharma P, Mahale A, Ghosh B, Kulkarni OP. Pharmacological blockade of HDAC3 accelerates diabetic wound healing by regulating macrophage activation. Life Sci. 2023;321:121574.
Not in our library10.1016/j.lfs.2023.121574
- 244.
Ghiboub M, Zhao J, Li Yim AYF, et al. HDAC3 mediates the inflammatory response and LPS tolerance in human monocytes and macrophages. Front Immunol. 2020;11:550769.
Not in our library10.3389/fimmu.2020.550769
- 245.
Xu L, An T, Jia B, et al. Histone deacetylase 3‐specific inhibitor RGFP966 attenuates oxidative stress and inflammation after traumatic brain injury by activating the Nrf2 pathway. Burns Trauma. 2024;12:tkad062.
Not in our library10.1093/burnst/tkad062
- 246.
Kang H, Kim S, Lee JY, Kim B. Inhibitory effects of ginsenoside compound K on lipopolysaccharide‐stimulated inflammatory responses in macrophages by regulating sirtuin 1 and histone deacetylase 4. Nutrients. 2023;15(7):1626.
Not in our library10.3390/nu15071626
- 247.
Kang H, Park YK, Lee JY. Inhibition of alcohol‐induced inflammation and oxidative stress by astaxanthin is mediated by its opposite actions in the regulation of sirtuin 1 and histone deacetylase 4 in macrophages. Biochim Biophys Acta Mol Cell Biol Lipids. 2021;1866(1):158838.
Not in our library10.1016/j.bbalip.2020.158838
- 248.
Zhao Y, Ma G, Yang X. HDAC5 promotes Mycoplasma pneumoniae‐induced inflammation in macrophages through NF‐κB activation. Life Sci. 2019;221:13‐19.
Not in our library10.1016/j.lfs.2019.02.004
- 249.
Poralla L, Stroh T, Erben U, et al. Histone deacetylase 5 regulates the inflammatory response of macrophages. J Cell Mol Med. 2015;19(9):2162‐2171.
Not in our library10.1111/jcmm.12595
- 250.
Yang X, Wang X, Liu D, Yu L, Xue B, Shi H. Epigenetic regulation of macrophage polarization by DNA methyltransferase 3b. Mol Endocrinol. 2014;28(4):565‐574.
Not in our library10.1210/me.2013-1293
- 251.
Li HD, Chen X, Xu JJ, et al. DNMT3b‐mediated methylation of ZSWIM3 enhances inflammation in alcohol‐induced liver injury via regulating TRAF2‐mediated NF‐κB pathway. Clin Sci (Lond). 2020;134(14):1935‐1956.
Not in our library10.1042/cs20200031
- 252.
Li B, Huo Y, Lin Z, Wang T. [DNA hydroxymethylase 10–11 translocation 2 (TET2) inhibits mouse macrophage activation and polarization]. Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2017;33(9):1165‐1170.
Not in our library
- 253.
Li C, Xu MM, Wang K, Adler AJ, Vella AT, Zhou B. Macrophage polarization and meta‐inflammation. Transl Res. 2018;191:29‐44.
Not in our library10.1016/j.trsl.2017.10.004
- 254.
Yu H, Pan J, Zheng S, et al. Hepatocellular carcinoma cell‐derived exosomal miR‐21‐5p induces macrophage M2 polarization by targeting RhoB. Int J Mol Sci. 2023;24(5):4593.
Not in our library10.3390/ijms24054593
- 255.
Wang Q, Xie Y, He Q, Geng Y, Xu J. LncRNA‐Cox2 regulates macrophage polarization and inflammatory response through the CREB‐C/EBPβ signaling pathway in septic mice. Int Immunopharmacol. 2021;101(Pt B):108347.
Not in our library10.1016/j.intimp.2021.108347
- 256.
- 257.
Chistiakov DA, Myasoedova VA, Revin VV, Orekhov AN, Bobryshev YV. The impact of interferon‐regulatory factors to macrophage differentiation and polarization into M1 and M2. Immunobiology. 2018;223(1):101‐111.
Not in our library10.1016/j.imbio.2017.10.005
- 258.
Zhu X, Guo Q, Zou J, et al. MiR‐19a‐3p suppresses M1 macrophage polarization by inhibiting STAT1/IRF1 pathway. Front Pharmacol. 2021;12:614044.
Not in our library10.3389/fphar.2021.614044
- 259.
Bian J, Zhu Y, Tian P, Yang Q, Li Z. Adaptor protein HIP‐55 promotes macrophage M1 polarization through promoting AP‐1 complex activation. Cell Signal. 2024;117:111124.
Not in our library10.1016/j.cellsig.2024.111124
- 260.
Tan S, Wang Z, Li N, et al. Transcription factor Zhx2 is a checkpoint that programs macrophage polarization and antitumor response. Cell Death Differ. 2023;30(9):2104‐2119.
Not in our library10.1038/s41418-023-01202-4
- 261.
Kroner A, Greenhalgh AD, Zarruk JG, Passos Dos Santos R, Gaestel M, David S. TNF and increased intracellular iron alter macrophage polarization to a detrimental M1 phenotype in the injured spinal cord. Neuron. 2014;83(5):1098‐1116.
Not in our library10.1016/j.neuron.2014.07.027
- 262.
Wang X, Cao Q, Yu L, Shi H, Xue B, Shi H. Epigenetic regulation of macrophage polarization and inflammation by DNA methylation in obesity. JCI Insight. 2016;1(19):e87748.
Not in our library10.1172/jci.insight.87748
- 263.
Tang RZ, Zhu JJ, Yang FF, et al. DNA methyltransferase 1 and Krüppel‐like factor 4 axis regulates macrophage inflammation and atherosclerosis. J Mol Cell Cardiol. 2019;128:11‐24.
Not in our library10.1016/j.yjmcc.2019.01.009
- 264.
Li J, Ye F, Xu X, et al. Targeting macrophage M1 polarization suppression through PCAF inhibition alleviates autoimmune arthritis via synergistic NF‐κB and H3K9Ac blockade. J Nanobiotechnology. 2023;21(1):280.
Not in our library10.1186/s12951-023-02012-z
- 265.
Mullican SE, Gaddis CA, Alenghat T, et al. Histone deacetylase 3 is an epigenomic brake in macrophage alternative activation. Genes Dev. 2011;25(23):2480‐2488.
Not in our library10.1101/gad.175950.111
- 266.
Zhou X, Chen H, Shi Y, et al. Histone deacetylase 8 inhibition prevents the progression of peritoneal fibrosis by counteracting the epithelial‐mesenchymal transition and blockade of M2 macrophage polarization. Front Immunol. 2023;14:1137332.
Not in our library10.3389/fimmu.2023.1137332
- 267.
Das Gupta K, Ramnath D, von Pein JB, et al. HDAC7 is an immunometabolic switch triaging danger signals for engagement of antimicrobial versus inflammatory responses in macrophages. Proc Natl Acad Sci USA. 2023;120(4):e2212813120.
Not in our library10.1073/pnas.2212813120
- 268.
Schiano C, Benincasa G, Franzese M, et al. Epigenetic‐sensitive pathways in personalized therapy of major cardiovascular diseases. Pharmacol Ther. 2020;210:107514.
Not in our library10.1016/j.pharmthera.2020.107514
- 269.
Zhong C, Tao B, Yang F, et al. Histone demethylase JMJD1C promotes the polarization of M1 macrophages to prevent glioma by upregulating miR‐302a. Clin Transl Med. 2021;11(9):e424.
Not in our library10.1002/ctm2.424
- 270.
Li H, Hu W, Lin Y, Xu T, Zhang X, Wang C. MicroRNA‐9‐5p is involved in lipopolysaccharide‐induced acute lung injury via the regulation of macrophage polarization. Int J Toxicol. 2023;42(2):156‐164.
Not in our library10.1177/10915818221146446
- 271.
- 272.
Zhang P, Wang H, Luo X, et al. MicroRNA‐155 inhibits polarization of macrophages to M2‐type and suppresses choroidal neovascularization. Inflammation. 2018;41(1):143‐153.
Not in our library10.1007/s10753-017-0672-8
- 273.
- 274.
Zhao C, Zeng N, Zhou X, et al. CAA‐derived IL‐6 induced M2 macrophage polarization by activating STAT3. BMC Cancer. 2023;23(1):392.
Not in our library10.1186/s12885-023-10826-1
- 275.
Liu M, Tong Z, Ding C, et al. Transcription factor c‐Maf is a checkpoint that programs macrophages in lung cancer. J Clin Invest. 2020;130(4):2081‐2096.
Not in our library10.1172/jci131335
- 276.
Li W, Wang Y, Zhu L, et al. The P300/XBP1s/Herpud1 axis promotes macrophage M2 polarization and the development of choroidal neovascularization. J Cell Mol Med. 2021;25(14):6709‐6720.
Not in our library10.1111/jcmm.16673
- 277.
denDekker AD, Davis FM, Joshi AD, et al. TNF‐α regulates diabetic macrophage function through the histone acetyltransferase MOF. JCI Insight. 2020;5(5):e132306.
Not in our library10.1172/jci.insight.132306
- 278.
Zhang M, Hei R, Zhou Z, Xiao W, Liu X, Chen Y. Macrophage polarization involved the inflammation of chronic obstructive pulmonary disease by S1P/HDAC1 signaling. Am J Cancer Res. 2023;13(9):4478‐4489.
Not in our library
- 279.
Zheng X, Sarode P, Weigert A, et al. The HDAC2‐SP1 axis orchestrates protumor macrophage polarization. Cancer Res. 2023;83(14):2345‐2357.
Not in our library10.1158/0008-5472.can-22-1270
- 280.
Xu G, Niu L, Wang Y, et al. HDAC6‐dependent deacetylation of TAK1 enhances sIL‐6R release to promote macrophage M2 polarization in colon cancer. Cell Death Dis. 2022;13(10):888.
Not in our library10.1038/s41419-022-05335-1
- 281.
Zhong Y, Huang T, Huang J, et al. The HDAC10 instructs macrophage M2 program via deacetylation of STAT3 and promotes allergic airway inflammation. Theranostics. 2023;13(11):3568‐3581.
Not in our library10.7150/thno.82535
- 282.
Luan B, Goodarzi MO, Phillips NG, et al. Leptin‐mediated increases in catecholamine signaling reduce adipose tissue inflammation via activation of macrophage HDAC4. Cell Metab. 2014;19(6):1058‐1065.
Not in our library10.1016/j.cmet.2014.03.024
- 283.
Peng W, Xie Y, Luo Z, et al. UTX deletion promotes M2 macrophage polarization by epigenetically regulating endothelial cell‐macrophage crosstalk after spinal cord injury. J Nanobiotechnology. 2023;21(1):225.
Not in our library10.1186/s12951-023-01986-0
- 284.
Lee JY, Mehrazarin S, Alshaikh A, et al. Histone Lys demethylase KDM3C demonstrates anti‐inflammatory effects by suppressing NF‐κB signaling and osteoclastogenesis. Faseb J. 2019;33(9):10515‐10527.
Not in our library10.1096/fj.201900154rr
- 285.
Liu T, Zhang Z, Shen W, Wu Y, Bian T. MicroRNA Let‐7 induces M2 macrophage polarization in COPD emphysema through the IL‐6/STAT3 pathway. Int J Chron Obstruct Pulmon Dis. 2023;18:575‐591.
Not in our library10.2147/copd.s404850
- 286.
Li Y, Chen X, Jin R, et al. Injectable hydrogel with MSNs/microRNA‐21‐5p delivery enables both immunomodification and enhanced angiogenesis for myocardial infarction therapy in pigs. Sci Adv. 2021;7(9):eabd6740.
Not in our library10.1126/sciadv.abd6740
- 287.
- 288.
Ghorbani S, Talebi F, Chan WF, et al. MicroRNA‐181 variants regulate T cell phenotype in the context of autoimmune neuroinflammation. Front Immunol. 2017;8:758.
Not in our library10.3389/fimmu.2017.00758
- 289.
Spinosa M, Lu G, Su G, et al. Human mesenchymal stromal cell‐derived extracellular vesicles attenuate aortic aneurysm formation and macrophage activation via microRNA‐147. Faseb J. 2018;32(11):fj201701138RR.
Not in our library10.1096/fj.201701138rr
- 290.
Wang Y, Han B, Wang Y, et al. Mesenchymal stem cell‐secreted extracellular vesicles carrying TGF‐β1 up‐regulate miR‐132 and promote mouse M2 macrophage polarization. J Cell Mol Med. 2020;24(21):12750‐12764.
Not in our library10.1111/jcmm.15860
- 291.
Freemerman AJ, Johnson AR, Sacks GN, et al. Metabolic reprogramming of macrophages: glucose transporter 1 (GLUT1)‐mediated glucose metabolism drives a proinflammatory phenotype. J Biol Chem. 2014;289(11):7884‐7896.
Not in our library10.1074/jbc.m113.522037
- 292.
Hou Y, Wei D, Zhang Z, et al. FABP5 controls macrophage alternative activation and allergic asthma by selectively programming long‐chain unsaturated fatty acid metabolism. Cell Rep. 2022;41(7):111668.
Not in our library10.1016/j.celrep.2022.111668
- 293.
- 294.
- 295.
Tardito S, Martinelli G, Soldano S, et al. Macrophage M1/M2 polarization and rheumatoid arthritis: a systematic review. Autoimmun Rev. 2019;18(11):102397.
Not in our library10.1016/j.autrev.2019.102397
- 296.
- 297.
- 298.
Du Y, Rong L, Cong Y, Shen L, Zhang N, Wang B. Macrophage polarization: an effective approach to targeted therapy of inflammatory bowel disease. Expert Opin Ther Targets. 2021;25(3):191‐209.
Not in our library10.1080/14728222.2021.1901079
- 299.
- 300.
Akkari L, Bowman RL, Tessier J, et al. Dynamic changes in glioma macrophage populations after radiotherapy reveal CSF‐1R inhibition as a strategy to overcome resistance. Sci Transl Med. 2020;12(552):eaaw7843.
Not in our library10.1126/scitranslmed.aaw7843
- 301.
Hu Q, Wu G, Wang R, Ma H, Zhang Z, Xue Q. Cutting edges and therapeutic opportunities on tumor‐associated macrophages in lung cancer. Front Immunol. 2022;13:1007812.
Not in our library10.3389/fimmu.2022.1007812
- 302.
Liu X, Hogg GD, Zuo C, et al. Context‐dependent activation of STING‐interferon signaling by CD11b agonists enhances anti‐tumor immunity. Cancer Cell. 2023;41(6):1073‐1090. e12.
Not in our library10.1016/j.ccell.2023.04.018
- 303.
Li LG, Yang XX, Xu HZ, et al. A dihydroartemisinin‐loaded nanoreactor motivates anti‐cancer immunotherapy by synergy‐induced ferroptosis to activate Cgas/STING for reprogramming of macrophage. Adv Healthc Mater. 2023;12(28):e2301561.
Not in our library10.1002/adhm.202301561
- 304.
Yu DM, Zhao J, Lee EE, et al. GLUT3 promotes macrophage signaling and function via RAS‐mediated endocytosis in atopic dermatitis and wound healing. J Clin Invest. 2023;133(21):e170706.
Not in our library10.1172/jci170706
- 305.
Shirakawa K, Endo J, Kataoka M, et al. IL (interleukin)‐10‐STAT3‐galectin‐3 axis is essential for osteopontin‐producing reparative macrophage polarization after myocardial infarction. Circulation. 2018;138(18):2021‐2035.
Not in our library10.1161/circulationaha.118.035047
- 306.
Zhang SM, Wei CY, Wang Q, Wang L, Lu L, Qi FZ. M2‐polarized macrophages mediate wound healing by regulating connective tissue growth factor via AKT, ERK1/2, and STAT3 signaling pathways. Mol Biol Rep. 2021;48(9):6443‐6456.
Not in our library10.1007/s11033-021-06646-w
- 307.
Gong T, Liu L, Jiang W, Zhou R. DAMP‐sensing receptors in sterile inflammation and inflammatory diseases. Nat Rev Immunol. 2020;20(2):95‐112.
Not in our library10.1038/s41577-019-0215-7
- 308.
Zindel J, Kubes P. DAMPs, PAMPs, and LAMPs in immunity and sterile inflammation. Annu Rev Pathol. 2020;15:493‐518.
Not in our library10.1146/annurev-pathmechdis-012419-032847
- 309.
- 310.
- 311.
- 312.
Tan F, Cao Y, Zheng L, et al. Diabetes exacerbated sepsis‐induced intestinal injury by promoting M1 macrophage polarization via miR‐3061/Snail1 signaling. Front Immunol. 2022;13:922614.
Not in our library10.3389/fimmu.2022.922614
- 313.
Wang E‐J, Wu M‐Y, Ren Z‐Y, et al. Targeting macrophage autophagy for inflammation resolution and tissue repair in inflammatory bowel disease. Burns Trauma. 2023;11:tkad004.
Not in our library10.1093/burnst/tkad004
- 314.
Boada‐Romero E, Martinez J, Heckmann BL, Green DR. The clearance of dead cells by efferocytosis. Nat Rev Mol Cell Biol. 2020;21(7):398‐414.
Not in our library10.1038/s41580-020-0232-1
- 315.
Yunna C, Mengru H, Lei W, Weidong C. Macrophage M1/M2 polarization. Eur J Pharmacol. 2020;877:173090.
Not in our library10.1016/j.ejphar.2020.173090
- 316.
Aderem A, Underhill DM. Mechanisms of phagocytosis in macrophages. Annu Rev Immunol. 1999;17:593‐623.
Not in our library10.1146/annurev.immunol.17.1.593
- 317.
- 318.
Small AG, Harvey S, Kaur J, et al. Vitamin D upregulates the macrophage complement receptor immunoglobulin in innate immunity to microbial pathogens. Commun Biol. 2021;4(1):401.
Not in our library10.1038/s42003-021-01943-3
- 319.
Minhas R, Bansal Y, Bansal G. Inducible nitric oxide synthase inhibitors: a comprehensive update. Med Res Rev. 2020;40(3):823‐855.
Not in our library10.1002/med.21636
- 320.
- 321.
Sivaraman K, Wrenger S, Liu B, et al. Mice inflammatory responses to inhaled aerosolized LPS: effects of various forms of human alpha1‐antitrypsin. J Leukoc Biol. 2023;113(1):58‐70.
Not in our library10.1093/jleuko/qiac004
- 322.
- 323.
Nagaoka I, Tamura H, Reich J. Therapeutic potential of cathelicidin peptide LL‐37, an antimicrobial agent, in a murine sepsis model. Int J Mol Sci. 2020;21(17):5973.
Not in our library10.3390/ijms21175973
- 324.
Szulc‐Dąbrowska L, Bossowska‐Nowicka M, Struzik J, Toka FN. Cathepsins in bacteria‐macrophage interaction: defenders or victims of circumstance? Front Cell Infect Microbiol. 2020;10:601072.
Not in our library10.3389/fcimb.2020.601072
- 325.
Weiss G, Schaible UE. Macrophage defense mechanisms against intracellular bacteria. Immunol Rev. 2015;264(1):182‐203.
Not in our library10.1111/imr.12266
- 326.
Rai R, Singh V, Mathew BJ, Singh AK, Chaurasiya SK. Mycobacterial response to an acidic environment: protective mechanisms. Pathog Dis. 2022;80(1):ftac032.
Not in our library10.1093/femspd/ftac032
- 327.
- 328.
Korobova ZR, Arsentieva NA, Totolian AA. Macrophage‐derived chemokine MDC/CCL22: an ambiguous finding in COVID‐19. Int J Mol Sci. 2023;24(17):13083.
Not in our library10.3390/ijms241713083
- 329.
Hurme P, Komulainen M, Tulkki M, et al. Cytokine expression in rhinovirus‐ vs. respiratory syncytial virus‐induced first wheezing episode and its relation to clinical course. Front Immunol. 2022;13:1044621.
Not in our library10.3389/fimmu.2022.1044621
- 330.
Jin H, Wen X, Sun R, et al. Engineered nanovesicles from activated neutrophils with enriched bactericidal proteins have molecular debridement ability and promote infectious wound healing. Burns Trauma. 2024;12:tkae018.
Not in our library10.1093/burnst/tkae018
- 331.
Mass E, Nimmerjahn F, Kierdorf K, Schlitzer A. Tissue‐specific macrophages: how they develop and choreograph tissue biology. Nat Rev Immunol. 2023;23(9):563‐579.
Not in our library10.1038/s41577-023-00848-y
- 332.
McCubbrey AL, McManus SA, McClendon JD, et al. Polyamine import and accumulation causes immunomodulation in macrophages engulfing apoptotic cells. Cell Rep. 2022;38(2):110222.
Not in our library10.1016/j.celrep.2021.110222
- 333.
Chang M, Nguyen TT. Strategy for treatment of infected diabetic foot ulcers. Acc Chem Res. 2021;54(5):1080‐1093.
Not in our library10.1021/acs.accounts.0c00864
- 334.
- 335.
Maassen S, Coenen B, Ioannidis M, et al. Itaconate promotes a wound resolving phenotype in pro‐inflammatory macrophages. Redox Biol. 2023;59:102591.
Not in our library10.1016/j.redox.2022.102591
- 336.
Zeng L, Zhou S, Chen C, et al. Experimental study of fat derived pellets promoting wound healing in rats. Bioengineered. 2021;12(2):12323‐12331.
Not in our library10.1080/21655979.2021.2000257
- 337.
Vannella KM, Wynn TA. Mechanisms of organ injury and repair by macrophages. Annu Rev Physiol. 2017;79:593‐617.
Not in our library10.1146/annurev-physiol-022516-034356
- 338.
Jung M, Ma Y, Iyer RP, et al. IL‐10 improves cardiac remodeling after myocardial infarction by stimulating M2 macrophage polarization and fibroblast activation. Basic Res Cardiol. 2017;112(3):33.
Not in our library10.1007/s00395-017-0622-5
- 339.
- 340.
Saraiva M, Vieira P, O'Garra A. Biology and therapeutic potential of interleukin‐10. J Exp Med. 2020;217(1):e20190418.
Not in our library10.1084/jem.20190418
- 341.
Minton K. Immune regulation: IL‐10 targets macrophage metabolism. Nat Rev Immunol. 2017;17(6):345.
Not in our library10.1038/nri.2017.57
- 342.
Wang J, Chen G, Li L, et al. Sustained induction of IP‐10 by MRP8/14 via the IFNβ–IRF7 axis in macrophages exaggerates lung injury in endotoxemic mice. Burns Trauma. 2023;11:tkad006.
Not in our library10.1093/burnst/tkad006
- 343.
Liu J, Wang H, Zhang L, et al. Periodontal ligament stem cells promote polarization of M2 macrophages. J Leukoc Biol. 2022;111(6):1185‐1197.
Not in our library10.1002/jlb.1ma1220-853rr
- 344.
- 345.
De Nardo D, Labzin LI, Kono H, et al. High‐density lipoprotein mediates anti‐inflammatory reprogramming of macrophages via the transcriptional regulator ATF3. Nat Immunol. 2014;15(2):152‐160.
Not in our library10.1038/ni.2784
- 346.
Petta I, Thorp M, Ciers M, et al. Myeloid A20 is critical for alternative macrophage polarization and type‐2 immune‐mediated helminth resistance. Front Immunol. 2024;15:1373745.
Not in our library10.3389/fimmu.2024.1373745
- 347.
Zheng Y, Wang S, Zhong Y, Huang C, Wu X. A20 affects macrophage polarization through the NLRP3 inflammasome signaling pathway and promotes breast cancer progression. Exp Ther Med. 2023;25(4):147.
Not in our library10.3892/etm.2023.11846
- 348.
Panigrahy D, Gilligan MM, Serhan CN, Kashfi K. Resolution of inflammation: an organizing principle in biology and medicine. Pharmacol Ther. 2021;227:107879.
Not in our library10.1016/j.pharmthera.2021.107879
- 349.
Martin P, Gurevich DB. Macrophage regulation of angiogenesis in health and disease. Semin Cell Dev Biol. 2021;119:101‐110.
Not in our library10.1016/j.semcdb.2021.06.010
- 350.
Hadrian K, Willenborg S, Bock F, Cursiefen C, Eming SA, Hos D. Macrophage‐mediated tissue vascularization: similarities and differences between cornea and skin. Front Immunol. 2021;12:667830.
Not in our library10.3389/fimmu.2021.667830
- 351.
Huang X, Zheng L, Zhou Y, et al. Controllable adaptive molybdate‐oligosaccharide nanoparticles regulate M2 macrophage mitochondrial function and promote angiogenesis via PI3K/HIF‐1α/VEGF pathway to accelerate diabetic wound healing. Adv Healthc Mater. 2024;13(3):e2302256.
Not in our library10.1002/adhm.202302256
- 352.
Du H, Li S, Lu J, et al. Single‐cell RNA‐seq and bulk‐seq identify RAB17 as a potential regulator of angiogenesis by human dermal microvascular endothelial cells in diabetic foot ulcers. Burns Trauma. 2023;11:tkad020.
Not in our library10.1093/burnst/tkad020
- 353.
Song X, Chen Y, Chen X, et al. Exosomes from tannic acid‐stimulated macrophages accelerate wound healing through miR‐221‐3p mediated fibroblasts migration by targeting CDKN1b. Int J Biol Macromol. 2023;244:125088.
Not in our library10.1016/j.ijbiomac.2023.125088
- 354.
Laplante P, Brillant‐Marquis F, Brissette MJ, et al. MFG‐E8 reprogramming of macrophages promotes wound healing by increased bFGF production and fibroblast functions. J Invest Dermatol. 2017;137(9):2005‐2013.
Not in our library10.1016/j.jid.2017.04.030
- 355.
- 356.
White MJV, Briquez PS, White DAV, Hubbell JA. VEGF‐A, PDGF‐BB and HB‐EGF engineered for promiscuous super affinity to the extracellular matrix improve wound healing in a model of type 1 diabetes. NPJ Regen Med. 2021;6(1):76.
Not in our library10.1038/s41536-021-00189-1
- 357.
Song Y, Yang J, Li T, et al. CD34(+) cell‐derived fibroblast‐macrophage cross‐talk drives limb ischemia recovery through the OSM‐ANGPTL signaling axis. Sci Adv. 2023;9(15):eadd2632.
Not in our library10.1126/sciadv.add2632
- 358.
Lapkina EZ, Esimbekova AR, Ruksha TG. [Vasculogenic mimicry]. Arkh Patol. 2023;85(6):62‐69.
Not in our library10.17116/patol20238506162
- 359.
Senk A, Fazzari J, Djonov V. Vascular mimicry in zebrafish fin regeneration: how macrophages build new blood vessels. Angiogenesis. 2024.
Not in our library10.1007/s10456-024-09914-y
- 360.
Yan D, He Y, Dai J, Yang L, Wang X, Ruan Q. Vascular endothelial growth factor modified macrophages transdifferentiate into endothelial‐like cells and decrease foam cell formation. Biosci Rep. 2017;37(3):BSR20170002.
Not in our library10.1042/bsr20170002
- 361.
Bai H, Xie B, Li M, et al. Biodegraded PCl and gelatin fabricated vascular patch in rat aortic and inferior vena cava angioplasty. Microvasc Res. 2022;141:104314.
Not in our library10.1016/j.mvr.2022.104314
- 362.
Forrest OA, Dobosh B, Ingersoll SA, et al. Neutrophil‐derived extracellular vesicles promote feed‐forward inflammasome signaling in cystic fibrosis airways. J Leukoc Biol. 2022;112(4):707‐716.
Not in our library10.1002/jlb.3ab0321-149r
- 363.
Talbott HE, Mascharak S, Griffin M, Wan DC, Longaker MT. Wound healing, fibroblast heterogeneity, and fibrosis. Cell Stem Cell. 2022;29(8):1161‐1180.
Not in our library10.1016/j.stem.2022.07.006
- 364.
- 365.
Shi T, Denney L, An H, Ho LP, Zheng Y. Alveolar and lung interstitial macrophages: definitions, functions, and roles in lung fibrosis. J Leukoc Biol. 2021;110(1):107‐114.
Not in our library10.1002/jlb.3ru0720-418r
- 366.
Wang J, Shang R, Yang J, et al. P311 promotes type II transforming growth factor‐β receptor mediated fibroblast activation and granulation tissue formation in wound healing. Burns Trauma. 2022;10:tkac027.
Not in our library10.1093/burnst/tkac027
- 367.
Wang Y, Zhang L, Wu GR, et al. MBD2 serves as a viable target against pulmonary fibrosis by inhibiting macrophage M2 program. Sci Adv. 2021;7(1):eabb6075.
Not in our library10.1126/sciadv.abb6075
- 368.
Huang C, Ogawa R. Role of inflammasomes in keloids and hypertrophic scars‐lessons learned from chronic diabetic wounds and skin fibrosis. Int J Mol Sci. 2022;23(12):6820.
Not in our library10.3390/ijms23126820
- 369.
- 370.
- 371.
- 372.
Zhu H, Fu J, Chen S, et al. FC‐99 reduces macrophage tenascin‐C expression by upregulating miRNA‐494 in arthritis. Int Immunopharmacol. 2020;79:106105.
Not in our library10.1016/j.intimp.2019.106105
- 373.
- 374.
Chen K, Rao Z, Dong S, et al. Roles of the fibroblast growth factor signal transduction system in tissue injury repair. Burns Trauma. 2022;10:tkac005.
Not in our library10.1093/burnst/tkac005
- 375.
Liu C, Pei M, Li Q, Zhang Y. Decellularized extracellular matrix mediates tissue construction and regeneration. Front Med. 2022;16(1):56‐82.
Not in our library10.1007/s11684-021-0900-3
- 376.
Huang J, Heng S, Zhang W, et al. Dermal extracellular matrix molecules in skin development, homeostasis, wound regeneration and diseases. Semin Cell Dev Biol. 2022;128:137‐144.
Not in our library10.1016/j.semcdb.2022.02.027
- 377.
Dai S, Xu M, Pang Q, et al. Hypoxia macrophage‐derived exosomal miR‐26b‐5p targeting PTEN promotes the development of keloids. Burns Trauma. 2024;12:tkad036.
Not in our library10.1093/burnst/tkad036
- 378.
- 379.
- 380.
Travnickova J, Nhim S, Abdellaoui N, et al. Macrophage morphological plasticity and migration is Rac signalling and MMP9 dependant. Sci Rep. 2021;11(1):10123.
Not in our library10.1038/s41598-021-88961-7
- 381.
Wang X, Zhang D, Fucci QA, Dollery CM, Owen CA. Surface‐bound matrix metalloproteinase‐8 on macrophages: Contributions to macrophage pericellular proteolysis and migration through tissue barriers. Physiol Rep. 2021;9(5):e14778.
Not in our library10.14814/phy2.14778
- 382.
Qiu L, Wang Y, Wang Y, et al. Ursolic acid ameliorated neuronal damage by restoring microglia‐activated MMP/TIMP imbalance in vitro. Drug Des Devel Ther. 2023;17:2481‐2493.
Not in our library10.2147/dddt.s411408
- 383.
Ishida Y, Kuninaka Y, Nosaka M, et al. Immunohistochemical analysis on MMP‐2 and MMP‐9 for wound age determination. Int J Legal Med. 2015;129(5):1043‐1048.
Not in our library10.1007/s00414-015-1167-5
- 384.
Cecchi R, Tomoya I, Camatti J, Mizuho N, Yuko I, Toshikazu K. Expression of matrix metalloproteinase‐9 (MMP‐9) in human skin within 1 hour after injury through immunohistochemical staining: a pilot study. Int J Legal Med. 2024.
Not in our library10.1007/s00414-024-03243-x
- 385.
Sun C, Yan H, Jiang K, Huang L. Protective effect of casticin on experimental skin wound healing of rats. J Surg Res. 2022;274:145‐152.
Not in our library10.1016/j.jss.2021.12.007
- 386.
Alonso‐Nocelo M, Ruiz‐Cañas L, Sancho P, et al. Macrophages direct cancer cells through a LOXL2‐mediated metastatic cascade in pancreatic ductal adenocarcinoma. Gut. 2023;72(2):345‐359.
Not in our library10.1136/gutjnl-2021-325564
- 387.
Chrobok NL, Sestito C, Wilhelmus MM, Drukarch B, van Dam AM. Is monocyte‐ and macrophage‐derived tissue transglutaminase involved in inflammatory processes? Amino Acids. 2017;49(3):441‐452.
Not in our library10.1007/s00726-016-2334-9
- 388.
Sun H, Kaartinen MT. Transglutaminases in monocytes and macrophages. Med Sci (Basel). 2018;6(4):115.
Not in our library10.3390/medsci6040115
- 389.
Kim SY, Nair MG. Macrophages in wound healing: activation and plasticity. Immunol Cell Biol. 2019;97(3):258‐267.
Not in our library10.1111/imcb.12236
- 390.
Xiong Y, Lin Z, Bu P, et al. A whole‐course‐repair system based on neurogenesis‐angiogenesis crosstalk and macrophage reprogramming promotes diabetic wound healing. Adv Mater. 2023;35(19):e2212300.
Not in our library10.1002/adma.202212300
- 391.
Wolf SJ, Melvin WJ, Gallagher K. Macrophage‐mediated inflammation in diabetic wound repair. Semin Cell Dev Biol. 2021;119:111‐118.
Not in our library10.1016/j.semcdb.2021.06.013
- 392.
Schlundt C, Fischer H, Bucher CH, Rendenbach C, Duda GN, Schmidt‐Bleek K. The multifaceted roles of macrophages in bone regeneration: a story of polarization, activation and time. Acta Biomater. 2021;133:46‐57.
Not in our library10.1016/j.actbio.2021.04.052
- 393.
- 394.
Miki S, Suzuki JI, Takashima M, Ishida M, Kokubo H, Yoshizumi M. S‐1‐Propenylcysteine promotes IL‐10‐induced M2c macrophage polarization through prolonged activation of IL‐10R/STAT3 signaling. Sci Rep. 2021;11(1):22469.
Not in our library10.1038/s41598-021-01866-3
- 395.
Selig M, Poehlman L, Lang NC, Völker M, Rolauffs B, Hart ML. Prediction of six macrophage phenotypes and their IL‐10 content based on single‐cell morphology using artificial intelligence. Front Immunol. 2023;14:1336393.
Not in our library10.3389/fimmu.2023.1336393
- 396.
Rahman K, Vengrenyuk Y, Ramsey SA, et al. Inflammatory Ly6Chi monocytes and their conversion to M2 macrophages drive atherosclerosis regression. J Clin Invest. 2017;127(8):2904‐2915.
Not in our library10.1172/jci75005
- 397.
Arnold L, Henry A, Poron F, et al. Inflammatory monocytes recruited after skeletal muscle injury switch into antiinflammatory macrophages to support myogenesis. J Exp Med. 2007;204(5):1057‐1069.
Not in our library10.1084/jem.20070075
- 398.
- 399.
Cui CY, Ferrucci L, Gorospe M. Macrophage involvement in aging‐associated skeletal muscle regeneration. Cells. 2023;12(9):1214.
Not in our library10.3390/cells12091214
- 400.
Scala P, Rehak L, Giudice V, et al. Stem cell and macrophage roles in skeletal muscle regenerative medicine. Int J Mol Sci. 2021;22(19):10867.
Not in our library10.3390/ijms221910867
- 401.
Wang Y, Lu J, Liu Y. Skeletal muscle regeneration in cardiotoxin‐induced muscle injury models. Int J Mol Sci. 2022;23(21):13380.
Not in our library10.3390/ijms232113380
- 402.
Li N, Chen J, Geng C, et al. Myoglobin promotes macrophage polarization to M1 type and pyroptosis via the RIG‐I/Caspase1/GSDMD signaling pathway in CS‐AKI. Cell Death Discov. 2022;8(1):90.
Not in our library10.1038/s41420-022-00894-w
- 403.
Martins L, Gallo CC, Honda TSB, et al. Skeletal muscle healing by M1‐like macrophages produced by transient expression of exogenous GM‐CSF. Stem Cell Res Ther. 2020;11(1):473.
Not in our library10.1186/s13287-020-01992-1
- 404.
Tonkin J, Temmerman L, Sampson RD, et al. Monocyte/macrophage‐derived IGF‐1 orchestrates murine skeletal muscle regeneration and modulates autocrine polarization. Mol Ther. 2015;23(7):1189‐1200.
Not in our library10.1038/mt.2015.66
- 405.
Kok HJ, Barton ER. Actions and interactions of IGF‐I and MMPs during muscle regeneration. Semin Cell Dev Biol. 2021;119:11‐22.
Not in our library10.1016/j.semcdb.2021.04.018
- 406.
Chowdary AR, Maerz T, Henn D, et al. Macrophage‐mediated PDGF activation correlates with regenerative outcomes following musculoskeletal trauma. Ann Surg. 2023;278(2):e349‐e359.
Not in our library10.1097/sla.0000000000005704
- 407.
Peck BD, Murach KA, Walton RG, et al. A muscle cell‐macrophage axis involving matrix metalloproteinase 14 facilitates extracellular matrix remodeling with mechanical loading. Faseb J. 2022;36(2):e22155.
Not in our library10.1096/fj.202100182rr
- 408.
Ratnayake D, Nguyen PD, Rossello FJ, et al. Macrophages provide a transient muscle stem cell niche via NAMPT secretion. Nature. 2021;591(7849):281‐287.
Not in our library10.1038/s41586-021-03199-7
- 409.
Shang M, Cappellesso F, Amorim R, et al. Macrophage‐derived glutamine boosts satellite cells and muscle regeneration. Nature. 2020;587(7835):626‐631.
Not in our library10.1038/s41586-020-2857-9
- 410.
Southerland KW, Xu Y, Peters DT, et al. Skeletal muscle regeneration failure in ischemic‐damaged limbs is associated with pro‐inflammatory macrophages and premature differentiation of satellite cells. Genome Med. 2023;15(1):95.
Not in our library10.1186/s13073-023-01250-y
- 411.
Tusavitz S, Keoonela S, Kalkstein M, et al. Macrophage‐derived Wnt signaling increases endothelial permeability during skeletal muscle injury. Inflamm Res. 2020;69(12):1235‐1244.
Not in our library10.1007/s00011-020-01397-z
- 412.
Campana L, Esser H, Huch M, Forbes S. Liver regeneration and inflammation: from fundamental science to clinical applications. Nat Rev Mol Cell Biol. 2021;22(9):608‐624.
Not in our library10.1038/s41580-021-00373-7
- 413.
Guilliams M, Scott CL. Liver macrophages in health and disease. Immunity. 2022;55(9):1515‐1529.
Not in our library10.1016/j.immuni.2022.08.002
- 414.
Liu R, Scimeca M, Sun Q, et al. Harnessing metabolism of hepatic macrophages to aid liver regeneration. Cell Death Dis. 2023;14(8):574.
Not in our library10.1038/s41419-023-06066-7
- 415.
- 416.
Li M, Sun X, Zhao J, et al. CCL5 deficiency promotes liver repair by improving inflammation resolution and liver regeneration through M2 macrophage polarization. Cell Mol Immunol. 2020;17(7):753‐764.
Not in our library10.1038/s41423-019-0279-0
- 417.
Li L, Cui L, Lin P, et al. Kupffer‐cell‐derived IL‐6 is repurposed for hepatocyte dedifferentiation via activating progenitor genes from injury‐specific enhancers. Cell Stem Cell. 2023;30(3):283‐299. e9.
Not in our library10.1016/j.stem.2023.01.009
- 418.
Li R, Li D, Nie Y. IL‐6/gp130 signaling: a key unlocking regeneration. Cell Regen. 2023;12(1):16.
Not in our library10.1186/s13619-023-00160-z
- 419.
Yang J, Mowry LE, Nejak‐Bowen KN, et al. β‐Catenin signaling in murine liver zonation and regeneration: a Wnt‐Wnt situation! Hepatology. 2014;60(3):964‐976.
Not in our library10.1002/hep.27082
- 420.
Hu S, Monga SP. Wnt/‐catenin signaling and liver regeneration: circuit, biology, and opportunities. Gene Expr. 2021;20(3):189‐199.
Not in our library10.3727/105221621x16111780348794
- 421.
Heo MJ, Suh JH, Poulsen KL, Ju C, Kim KH. Updates on the immune cell basis of hepatic ischemia‐reperfusion injury. Mol Cells. 2023;46(9):527‐534.
Not in our library10.14348/molcells.2023.0099
- 422.
- 423.
- 424.
Liu Z, Wang M, Wang X, et al. XBP1 deficiency promotes hepatocyte pyroptosis by impairing mitophagy to activate mtDNA‐cGAS‐STING signaling in macrophages during acute liver injury. Redox Biol. 2022;52:102305.
Not in our library10.1016/j.redox.2022.102305
- 425.
- 426.
Yap J, Irei J, Lozano‐Gerona J, Vanapruks S, Bishop T, Boisvert WA. Macrophages in cardiac remodelling after myocardial infarction. Nat Rev Cardiol. 2023;20(6):373‐385.
Not in our library10.1038/s41569-022-00823-5
- 427.
- 428.
Chen Y, Wu G, Li M, et al. LDHA‐mediated metabolic reprogramming promoted cardiomyocyte proliferation by alleviating ROS and inducing M2 macrophage polarization. Redox Biol. 2022;56:102446.
Not in our library10.1016/j.redox.2022.102446
- 429.
- 430.
Jian Y, Zhou X, Shan W, et al. Crosstalk between macrophages and cardiac cells after myocardial infarction. Cell Commun Signal. 2023;21(1):109.
Not in our library10.1186/s12964-023-01105-4
- 431.
Thorp EB. Cardiac macrophages and emerging roles for their metabolism after myocardial infarction. J Clin Invest. 2023;133(18):e171953.
Not in our library10.1172/jci171953
- 432.
- 433.
Jiang C, Jin X, Li C, et al. Roles of IL‐33 in the pathogenesis of cardiac disorders. Exp Biol Med (Maywood). 2023;248(22):2167‐2174.
Not in our library10.1177/15353702231198075
- 434.
Li Z, Liu X, Zhang X, et al. TRIM21 aggravates cardiac injury after myocardial infarction by promoting M1 macrophage polarization. Front Immunol. 2022;13:1053171.
Not in our library10.3389/fimmu.2022.1053171
- 435.
Zha Z, Cheng Y, Cao L, et al. Monomeric CRP aggravates myocardial injury after myocardial infarction by polarizing the macrophage to pro‐inflammatory phenotype through JNK signaling pathway. J Inflamm Res. 2021;14:7053‐7064.
Not in our library10.2147/jir.s316816
- 436.
- 437.
- 438.
Monavarian M, Kader S, Moeinzadeh S, Jabbari E. Regenerative scar‐free skin wound healing. Tissue Eng Part B Rev. 2019;25(4):294‐311.
Not in our library10.1089/ten.teb.2018.0350
- 439.
Hong YK, Chang YH, Lin YC, Chen B, Guevara BEK, Hsu CK. Inflammation in wound healing and pathological scarring. Adv Wound Care (New Rochelle). 2023;12(5):288‐300.
Not in our library10.1089/wound.2021.0161
- 440.
Ullm F, Riedl P, Machado de Amorim A, et al. 3D scaffold‐based macrophage fibroblast coculture model reveals IL‐10 dependence of wound resolution phase. Adv Biosyst. 2020;4(1):e1900220.
Not in our library10.1002/adbi.201900220
- 441.
Wu R, Zhang H, Zhao M, et al. Nrf2 in keratinocytes protects against skin fibrosis via regulating epidermal lesion and inflammatory response. Biochem Pharmacol. 2020;174:113846.
Not in our library10.1016/j.bcp.2020.113846
- 442.
Villarreal‐Ponce A, Tiruneh MW, Lee J, et al. Keratinocyte‐macrophage crosstalk by the Nrf2/Ccl2/EGF signaling axis orchestrates tissue repair. Cell Rep. 2020;33(8):108417.
Not in our library10.1016/j.celrep.2020.108417
- 443.
Sen CK. Human wound and its burden: updated 2022 compendium of estimates. Adv Wound Care (New Rochelle). 2023;12(12):657‐670.
Not in our library10.1089/wound.2023.0150
- 444.
- 445.
Armstrong DG, Tan TW, Boulton AJM, Bus SA. Diabetic foot ulcers: a review. Jama. 2023;330(1):62‐75.
Not in our library10.1001/jama.2023.10578
- 446.
McDermott K, Fang M, Boulton AJM, Selvin E, Hicks CW. Etiology, epidemiology, and disparities in the burden of diabetic foot ulcers. Diabetes Care. 2023;46(1):209‐221.
Not in our library10.2337/dci22-0043
- 447.
Papachristou S, Pafili K, Papanas N. Skin AGEs and diabetic neuropathy. BMC Endocr Disord. 2021;21(1):28.
Not in our library10.1186/s12902-021-00697-7
- 448.
Harb A, Elbatreek MH, Elshahat A, El‐Akabawy N, Barakat W, Elkomy NM. Repurposing alagebrium for diabetic foot ulcer healing: impact on AGEs/NFκB/NOX1 signaling. Eur J Pharmacol. 2023;959:176083.
Not in our library10.1016/j.ejphar.2023.176083
- 449.
Shomali N, Mahmoudi J, Mahmoodpoor A, et al. Harmful effects of high amounts of glucose on the immune system: an updated review. Biotechnol Appl Biochem. 2021;68(2):404‐410.
Not in our library10.1002/bab.1938
- 450.
Aki T, Funakoshi T, Noritake K, Unuma K, Uemura K. Extracellular glucose is crucially involved in the fate decision of LPS‐stimulated RAW264.7 murine macrophage cells. Sci Rep. 2020;10(1):10581.
Not in our library10.1038/s41598-020-67396-6
- 451.
Kaewarpai T, Thongboonkerd V. High‐glucose‐induced changes in macrophage secretome: regulation of immune response. Mol Cell Biochem. 2019;452(1‐2):51‐62.
Not in our library10.1007/s11010-018-3411-z
- 452.
An Y, Zhang H, Wang C, et al. Activation of ROS/MAPKs/NF‐κB/NLRP3 and inhibition of efferocytosis in osteoclast‐mediated diabetic osteoporosis. Faseb J. 2019;33(11):12515‐12527.
Not in our library10.1096/fj.201802805rr
- 453.
Mo Y, Mo L, Zhang Y, Zhang Y, Yuan J, Zhang Q. High glucose enhances the activation of NLRP3 inflammasome by ambient fine particulate matter in alveolar macrophages. Part Fibre Toxicol. 2023;20(1):41.
Not in our library10.1186/s12989-023-00552-8
- 454.
He W, Mu X, Wu X, et al. The cGAS‐STING pathway: a therapeutic target in diabetes and its complications. Burns Trauma. 2024;12:tkad050.
Not in our library10.1093/burnst/tkad050
- 455.
Geng K, Ma X, Jiang Z, et al. High glucose‐induced STING activation inhibits diabetic wound healing through promoting M1 polarization of macrophages. Cell Death Discov. 2023;9(1):136.
Not in our library10.1038/s41420-023-01425-x
- 456.
Zhao Z, Ming Y, Li X, et al. Hyperglycemia aggravates periodontitis via autophagy impairment and ros‐inflammasome‐mediated macrophage pyroptosis. Int J Mol Sci. 2023;24(7):6309.
Not in our library10.3390/ijms24076309
- 457.
Suzuki T, Yamashita S, Hattori K, Matsuda N, Hattori Y. Impact of a long‐term high‐glucose environment on pro‐inflammatory responses in macrophages stimulated with lipopolysaccharide. Naunyn Schmiedebergs Arch Pharmacol. 2021;394(10):2129‐2139.
Not in our library10.1007/s00210-021-02137-8
- 458.
Yuan Y, Chen Y, Peng T, et al. Mitochondrial ROS‐induced lysosomal dysfunction impairs autophagic flux and contributes to M1 macrophage polarization in a diabetic condition. Clin Sci (Lond). 2019;133(15):1759‐1777.
Not in our library10.1042/cs20190672
- 459.
- 460.
Shaikh‐Kader A, Houreld NN, Rajendran NK, Abrahamse H. The link between advanced glycation end products and apoptosis in delayed wound healing. Cell Biochem Funct. 2019;37(6):432‐442.
Not in our library10.1002/cbf.3424
- 461.
Parthasarathy G, Mauer AS, Golla N, et al. Macrophage RAGE activation is proinflammatory in NASH. JCI Insight. 2024;9(3):e169138.
Not in our library10.1172/jci.insight.169138
- 462.
- 463.
Leerach N, Munesue S, Harashima A, et al. RAGE signaling antagonist suppresses mouse macrophage foam cell formation. Biochem Biophys Res Commun. 2021;555:74‐80.
Not in our library10.1016/j.bbrc.2021.03.139
- 464.
Li K, Chen G, Luo H, et al. MRP8/14 mediates macrophage efferocytosis through RAGE and Gas6/MFG‐E8, and induces polarization via TLR4‐dependent pathway. J Cell Physiol. 2021;236(2):1375‐1390.
Not in our library10.1002/jcp.29944
- 465.
Fu J, Sun Z, Wang X, et al. The single‐cell landscape of kidney immune cells reveals transcriptional heterogeneity in early diabetic kidney disease. Kidney Int. 2022;102(6):1291‐1304.
Not in our library10.1016/j.kint.2022.08.026
- 466.
Jia Y, Chen J, Zheng Z, et al. Tubular epithelial cell‐derived extracellular vesicles induce macrophage glycolysis by stabilizing HIF‐1α in diabetic kidney disease. Mol Med. 2022;28(1):95.
Not in our library10.1186/s10020-022-00525-1
- 467.
Codo AC, Davanzo GG, Monteiro LB, et al. Elevated glucose levels favor SARS‐CoV‐2 infection and monocyte response through a HIF‐1α/glycolysis‐dependent axis. Cell Metab. 2020;32(3):437‐446. e5.
Not in our library10.1016/j.cmet.2020.07.007
- 468.
Wang Q, Zhong Y, Li Z, et al. Multitranscriptome analyses of keloid fibroblasts reveal the role of the HIF‐1α/HOXC6/ERK axis in keloid development. Burns Trauma. 2022;10:tkac013.
Not in our library10.1093/burnst/tkac013
- 469.
Hull RP, Srivastava PK, D'Souza Z, et al. Combined ChIP‐Seq and transcriptome analysis identifies AP‐1/JunD as a primary regulator of oxidative stress and IL‐1β synthesis in macrophages. BMC Genomics. 2013;14:92.
Not in our library10.1186/1471-2164-14-92
- 470.
Kim NY, Kim S, Park HM, et al. Cinnamomum verum extract inhibits NOX2/ROS and PKCδ/JNK/AP‐1/NF‐κB pathway‐mediated inflammatory response in PMA‐stimulated THP‐1 monocytes. Phytomedicine. 2023;112:154685.
Not in our library10.1016/j.phymed.2023.154685
- 471.
Liu J, Wei Y, Jia W, et al. Chenodeoxycholic acid suppresses AML progression through promoting lipid peroxidation via ROS/p38 MAPK/DGAT1 pathway and inhibiting M2 macrophage polarization. Redox Biol. 2022;56:102452.
Not in our library10.1016/j.redox.2022.102452
- 472.
- 473.
Zhai Z, Gomez‐Mejiba SE, Gimenez MS, et al. Free radical‐operated proteotoxic stress in macrophages primed with lipopolysaccharide. Free Radic Biol Med. 2012;53(1):172‐181.
Not in our library10.1016/j.freeradbiomed.2012.04.023
- 474.
Liu Z, Ma Y, Cui Q, et al. Toll‐like receptor 4 plays a key role in advanced glycation end products‐induced M1 macrophage polarization. Biochem Biophys Res Commun. 2020;531(4):602‐608.
Not in our library10.1016/j.bbrc.2020.08.014
- 475.
- 476.
He S, Hu Q, Xu X, et al. Advanced glycation end products enhance M1 macrophage polarization by activating the MAPK pathway. Biochem Biophys Res Commun. 2020;525(2):334‐340.
Not in our library10.1016/j.bbrc.2020.02.053
- 477.
Xing Y, Pan S, Zhu L, et al. Advanced glycation end products induce atherosclerosis via RAGE/TLR4 signaling mediated‐m1 macrophage polarization‐dependent vascular smooth muscle cell phenotypic conversion. Oxid Med Cell Longev. 2022;2022:9763377.
Not in our library10.1155/2022/9763377
- 478.
Itakura M, Yamaguchi K, Kitazawa R, et al. Histone functions as a cell‐surface receptor for AGEs. Nat Commun. 2022;13(1):2974.
Not in our library10.1038/s41467-022-30626-8
- 479.
Ju CC, Liu XX, Liu LH, et al. Epigenetic modification: a novel insight into diabetic wound healing. Heliyon. 2024;10(6):e28086.
Not in our library10.1016/j.heliyon.2024.e28086
- 480.
Mir AR, Habib S, Uddin M. Recent advances in histone glycation: emerging role in diabetes and cancer. Glycobiology. 2021;31(9):1072‐1079.
Not in our library10.1093/glycob/cwab011
- 481.
Mao QY, He SY, Hu QY, et al. Advanced glycation end products (AGEs) inhibit macrophage efferocytosis of apoptotic β cells through binding to the receptor for AGEs. J Immunol. 2022;208(5):1204‐1213.
Not in our library10.4049/jimmunol.2100695
- 482.
Friggeri A, Banerjee S, Biswas S, et al. Participation of the receptor for advanced glycation end products in efferocytosis. J Immunol. 2011;186(11):6191‐6198.
Not in our library10.4049/jimmunol.1004134
- 483.
Zayed MA, Wei X, Park KM, et al. N‐Acetylcysteine accelerates amputation stump healing in the setting of diabetes. Faseb J. 2017;31(6):2686‐2695.
Not in our library10.1096/fj.201601348r
- 484.
Afzali H, Jafari Kashi AH, Momen‐Heravi M, et al. The effects of magnesium and vitamin E co‐supplementation on wound healing and metabolic status in patients with diabetic foot ulcer: A randomized, double‐blind, placebo‐controlled trial. Wound Repair Regen. 2019;27(3):277‐284.
Not in our library10.1111/wrr.12701
- 485.
Saeg F, Orazi R, Bowers GM, Janis JE. Evidence‐based nutritional interventions in wound care. Plast Reconstr Surg. 2021;148(1):226‐238.
Not in our library10.1097/prs.0000000000008061
- 486.
Nikolic M, Andjic M, Bradic J, et al. Topical application of siberian pine essential oil formulations enhance diabetic wound healing. Pharmaceutics. 2023;15(10):2437.
Not in our library10.3390/pharmaceutics15102437
- 487.
Eghtedari Y, Oh LJ, Girolamo ND, Watson SL. The role of topical N‐acetylcysteine in ocular therapeutics. Surv Ophthalmol. 2022;67(2):608‐622.
Not in our library10.1016/j.survophthal.2021.07.008
- 488.
Tian M, Qing C, Niu Y, et al. Effect of aminoguanidine intervention on neutrophils in diabetes inflammatory cells wound healing. Exp Clin Endocrinol Diabetes. 2013;121(10):635‐642.
Not in our library10.1055/s-0033-1351331
- 489.
Jiang M, Yakupu A, Guan H, et al. Pyridoxamine ameliorates methylglyoxal‐induced macrophage dysfunction to facilitate tissue repair in diabetic wounds. Int Wound J. 2022;19(1):52‐63.
Not in our library10.1111/iwj.13597
- 490.
Chang PC, Tsai SC, Jheng YH, Lin YF, Chen CC. Soft‐tissue wound healing by anti‐advanced glycation end‐products agents. J Dent Res. 2014;93(4):388‐393.
Not in our library10.1177/0022034514523785
- 491.
Kim CH, Kang HY, Kim G, et al. Soluble receptors for advanced glycation end‐products prevent unilateral ureteral obstruction‐induced renal fibrosis. Front Pharmacol. 2023;14:1172269.
Not in our library10.3389/fphar.2023.1172269
- 492.
Miyagawa T, Iwata Y, Oshima M, et al. Soluble receptor for advanced glycation end products protects from ischemia‐ and reperfusion‐induced acute kidney injury. Biol Open. 2022;11(1):bio058852.
Not in our library10.1242/bio.058852
- 493.
- 494.
Ding Y, Yang P, Li S, Zhang H, Ding X, Tan Q. Resveratrol accelerates wound healing by inducing M2 macrophage polarisation in diabetic mice. Pharm Biol. 2022;60(1):2328‐2337.
Not in our library10.1080/13880209.2022.2149821
- 495.
Qing L, Fu J, Wu P, Zhou Z, Yu F, Tang J. Metformin induces the M2 macrophage polarization to accelerate the wound healing via regulating AMPK/mTOR/NLRP3 inflammasome singling pathway. Am J Transl Res. 2019;11(2):655‐668.
Not in our library
- 496.
Cavalcante‐Silva J, Koh TJ. Targeting the NOD‐Like receptor pyrin domain containing 3 inflammasome to improve healing of diabetic wounds. Adv Wound Care (New Rochelle). 2023;12(11):644‐656.
Not in our library10.1089/wound.2021.0148
- 497.
Tawfeek HM, Abou‐Taleb DAE, Badary DM, Ibrahim M, Abdellatif AAH. Pharmaceutical, clinical, and immunohistochemical studies of metformin hydrochloride topical hydrogel for wound healing application. Arch Dermatol Res. 2020;312(2):113‐121.
Not in our library10.1007/s00403-019-01982-1
- 498.
- 499.
Liu Y, Zhang Z, Wang B, et al. Inflammation‐stimulated MSC‐derived small extracellular vesicle miR‐27b‐3p regulates macrophages by targeting CSF‐1 to promote temporomandibular joint condylar regeneration. Small. 2022;18(16):e2107354.
Not in our library10.1002/smll.202107354
- 500.
Ead JK, Armstrong DG. Granulocyte‐macrophage colony‐stimulating factor: conductor of the wound healing orchestra? Int Wound J. 2023;20(4):1229‐1234.
Not in our library10.1111/iwj.13919
- 501.
Freuchet A, Salama A, Remy S, Guillonneau C, Anegon I. IL‐34 and CSF‐1, deciphering similarities and differences at steady state and in diseases. J Leukoc Biol. 2021;110(4):771‐796.
Not in our library10.1002/jlb.3ru1120-773r
- 502.
- 503.
Wei Y, Li J, Huang Y, et al. The clinical effectiveness and safety of using epidermal growth factor, fibroblast growth factor and granulocyte‐macrophage colony stimulating factor as therapeutics in acute skin wound healing: a systematic review and meta‐analysis. Burns Trauma. 2022;10:tkac002.
Not in our library10.1093/burnst/tkac002
- 504.
Wang LL, Zhao R, Li JY, et al. Pharmacological activation of cannabinoid 2 receptor attenuates inflammation, fibrogenesis, and promotes re‐epithelialization during skin wound healing. Eur J Pharmacol. 2016;786:128‐136.
Not in our library10.1016/j.ejphar.2016.06.006
- 505.
Ma C, Ouyang Q, Huang Z, et al. Toll‐like receptor 9 inactivation alleviated atherosclerotic progression and inhibited macrophage polarized to M1 phenotype in ApoE‐/‐ mice. Dis Markers. 2015;2015:909572.
Not in our library10.1155/2015/909572
- 506.
Schmitt H, Ulmschneider J, Billmeier U, et al. The TLR9 agonist cobitolimod induces IL10‐Producing wound healing macrophages and regulatory T cells in ulcerative colitis. J Crohns Colitis. 2020;14(4):508‐524.
Not in our library10.1093/ecco-jcc/jjz170
- 507.
Gao Y, Jin H, Tan H, Cai X, Sun Y. Erythrocyte‐derived extracellular vesicles aggravate inflammation by promoting the proinflammatory macrophage phenotype through TLR4‐MyD88‐NF‐κB‐MAPK pathway. J Leukoc Biol. 2022;112(4):693‐706.
Not in our library10.1002/jlb.3a0821-451rr
- 508.
Akter S, Sharma RK, Sharma S, Rastogi S, Fiebich BL, Akundi RS. Exogenous ATP modulates PGE(2) release in macrophages through sustained phosphorylation of CDK9 and p38 MAPK. J Leukoc Biol. 2021;110(4):663‐677.
Not in our library10.1002/jlb.3a1219-697rr
- 509.
Gao S, Li L, Li L, et al. Effects of the combination of tanshinone IIA and puerarin on cardiac function and inflammatory response in myocardial ischemia mice. J Mol Cell Cardiol. 2019;137:59‐70.
Not in our library10.1016/j.yjmcc.2019.09.012
- 510.
Wu J, Ma X, Lu Y, et al. Edible pueraria lobata‐derived exosomes promote M2 macrophage polarization. Molecules. 2022;27(23):8184.
Not in our library10.3390/molecules27238184
- 511.
Luo Z, Qi B, Sun Y, et al. Engineering bioactive M2 macrophage‐polarized, anti‐inflammatory, miRNA‐based liposomes for functional muscle repair: from exosomal mechanisms to biomaterials. Small. 2022;18(34):e2201957.
Not in our library10.1002/smll.202201957
- 512.
Li J, Wei C, Yang Y, Gao Z, Guo Z, Qi F. Apoptotic bodies extracted from adipose mesenchymal stem cells carry microRNA‐21‐5p to induce M2 polarization of macrophages and augment skin wound healing by targeting KLF6. Burns. 2022;48(8):1893‐1908.
Not in our library10.1016/j.burns.2021.12.010
- 513.
Zhou LS, Zhao GL, Liu Q, Jiang SC, Wang Y, Zhang DM. Silencing collapsin response mediator protein‐2 reprograms macrophage phenotype and improves infarct healing in experimental myocardial infarction model. J Inflamm (Lond). 2015;12:11.
Not in our library10.1186/s12950-015-0053-8
- 514.
Danon D, Madjar J, Edinov E, et al. Treatment of human ulcers by application of macrophages prepared from a blood unit. Exp Gerontol. 1997;32(6):633‐641.
Not in our library10.1016/s0531-5565(97)00094-6
- 515.
Lopes TCM, Almeida GG, Souza IA, et al. High‐density‐immune‐complex regulatory macrophages promote recovery of experimental colitis in mice. Inflammation. 2021;44(3):1069‐1082.
Not in our library10.1007/s10753-020-01403-w
- 516.
Zheng D, Wang Y, Cao Q, et al. Transfused macrophages ameliorate pancreatic and renal injury in murine diabetes mellitus. Nephron Exp Nephrol. 2011;118(4):e87‐e99.
Not in our library10.1159/000321034
- 517.
Theocharidis G, Rahmani S, Lee S, et al. Murine macrophages or their secretome delivered in alginate dressings enhance impaired wound healing in diabetic mice. Biomaterials. 2022;288:121692.
Not in our library10.1016/j.biomaterials.2022.121692
- 518.
Whitaker R, Hernaez‐Estrada B, Hernandez RM, Santos‐Vizcaino E, Spiller KL. Immunomodulatory biomaterials for tissue repair. Chem Rev. 2021;121(18):11305‐11335.
Not in our library10.1021/acs.chemrev.0c00895
- 519.
Das P, Manna S, Roy S, Nandi SK, Basak P. Polymeric biomaterials‐based tissue engineering for wound healing: a systemic review. Burns Trauma. 2023;11:tkac058.
Not in our library10.1093/burnst/tkac058
- 520.
- 521.
Martin KE, García AJ. Macrophage phenotypes in tissue repair and the foreign body response: Implications for biomaterial‐based regenerative medicine strategies. Acta Biomater. 2021;133:4‐16.
Not in our library10.1016/j.actbio.2021.03.038
- 522.
Huang YY, Lin CW, Cheng NC, et al. Effect of a novel macrophage‐regulating drug on wound healing in patients with diabetic foot ulcers: a randomized clinical trial. JAMA Netw Open. 2021;4(9):e2122607.
Not in our library10.1001/jamanetworkopen.2021.22607
- 523.
Wu Y, Zhang J, Lin A, et al. Immunomodulatory poly(L‐lactic acid) nanofibrous membranes promote diabetic wound healing by inhibiting inflammation, oxidation and bacterial infection. Burns Trauma. 2024;12:tkae009.
Not in our library10.1093/burnst/tkae009
- 524.
- 525.
Kwak G, Cheng J, Kim H, et al. Sustained exosome‐guided macrophage polarization using hydrolytically degradable PEG hydrogels for cutaneous wound healing: identification of key proteins and MiRNAs, and sustained release formulation. Small. 2022;18(15):e2200060.
Not in our library10.1002/smll.202200060
- 526.
Shen P, Chen Y, Luo S, et al. Applications of biomaterials for immunosuppression in tissue repair and regeneration. Acta Biomater. 2021;126:31‐44.
Not in our library10.1016/j.actbio.2021.03.019
- 527.
Huang K, Liu W, Wei W, et al. Photothermal hydrogel encapsulating intelligently bacteria‐capturing Bio‐MOF for infectious wound healing. ACS Nano. 2022;16(11):19491‐19508.
Not in our library10.1021/acsnano.2c09593
- 528.
Henn D, Chen K, Fehlmann T, et al. Xenogeneic skin transplantation promotes angiogenesis and tissue regeneration through activated Trem2(+) macrophages. Sci Adv. 2021;7(49):eabi4528.
Not in our library10.1126/sciadv.abi4528
- 529.
Tu C, Lu H, Zhou T, et al. Promoting the healing of infected diabetic wound by an anti‐bacterial and nano‐enzyme‐containing hydrogel with inflammation‐suppressing, ROS‐scavenging, oxygen and nitric oxide‐generating properties. Biomaterials. 2022;286:121597.
Not in our library10.1016/j.biomaterials.2022.121597
- 530.
Chen Z, Wang L, Guo C, et al. Vascularized polypeptide hydrogel modulates macrophage polarization for wound healing. Acta Biomater. 2023;155:218‐234.
Not in our library10.1016/j.actbio.2022.11.002
- 531.
Zhao R, Jin X, Li A, et al. Precise diabetic wound therapy: PLS nanospheres eliminate senescent cells via DPP4 targeting and PARP1 activation. Adv Sci (Weinh). 2022;9(1):e2104128.
Not in our library10.1002/advs.202104128
- 532.
Liu W, Zu L, Wang S, et al. Tailored biomedical materials for wound healing. Burns Trauma. 2023;11:tkad040.
Not in our library10.1093/burnst/tkad040
- 533.
Huang Y, Zhang L, Song R, Mao X, Tang S. A carrageenan/agarose composite sponge and its immunomodulatory activities toward RAW264.7. J Biomed Mater Res A. 2021;109(6):829‐839.
Not in our library10.1002/jbm.a.37070
- 534.
Yang H, Song L, Sun B, et al. Modulation of macrophages by a paeoniflorin‐loaded hyaluronic acid‐based hydrogel promotes diabetic wound healing. Mater Today Bio. 2021;12:100139.
Not in our library10.1016/j.mtbio.2021.100139
- 535.
Wu J, Chen A, Zhou Y, et al. Novel H(2)S‐Releasing hydrogel for wound repair via in situ polarization of M2 macrophages. Biomaterials. 2019;222:119398.
Not in our library10.1016/j.biomaterials.2019.119398
- 536.
Saleh B, Dhaliwal HK, Portillo‐Lara R, et al. Local immunomodulation using an adhesive hydrogel loaded with miRNA‐laden nanoparticles promotes wound healing. Small. 2019;15(36):e1902232.
Not in our library10.1002/smll.201902232
- 537.
Chu D, Chen J, Liu X, et al. A tetramethylpyrazine‐loaded hyaluronic acid‐based hydrogel modulates macrophage polarization for promoting wound recovery in diabetic mice. Int J Biol Macromol. 2023;245:125495.
Not in our library10.1016/j.ijbiomac.2023.125495
- 538.
- 539.
Zhou Z, Deng T, Tao M, et al. Snail‐inspired AFG/GelMA hydrogel accelerates diabetic wound healing via inflammatory cytokines suppression and macrophage polarization. Biomaterials. 2023;299:122141.
Not in our library10.1016/j.biomaterials.2023.122141
- 540.
Shen T, Dai K, Yu Y, Wang J, Liu C. Sulfated chitosan rescues dysfunctional macrophages and accelerates wound healing in diabetic mice. Acta Biomater. 2020;117:192‐203.
Not in our library10.1016/j.actbio.2020.09.035
- 541.
Zhang S, Liu Y, Zhang X, et al. Prostaglandin E(2) hydrogel improves cutaneous wound healing via M2 macrophages polarization. Theranostics. 2018;8(19):5348‐5361.
Not in our library10.7150/thno.27385
- 542.
Sheng W, Qin H, Wang T, et al. Advanced phosphocreatine‐grafted chitosan hydrogel promote wound healing by macrophage modulation. Front Bioeng Biotechnol. 2023;11:1199939.
Not in our library10.3389/fbioe.2023.1199939
- 543.
Geng X, Qi Y, Liu X, Shi Y, Li H, Zhao L. A multifunctional antibacterial and self‐healing hydrogel laden with bone marrow mesenchymal stem cell‐derived exosomes for accelerating diabetic wound healing. Biomater Adv. 2022;133:112613.
Not in our library10.1016/j.msec.2021.112613
- 544.
Kong X, Chen H, Li F, et al. Three‐dimension chitosan hydrogel loading melanin composite nanoparticles for wound healing by anti‐bacteria, immune activation and macrophage autophagy promotion. Int J Biol Macromol. 2023;237:124176.
Not in our library10.1016/j.ijbiomac.2023.124176
- 545.
Vivcharenko V, Wojcik M, Przekora A. Cellular response to vitamin C‐enriched chitosan/agarose film with potential application as artificial skin substitute for chronic wound treatment. Cells. 2020;9(5):1185.
Not in our library10.3390/cells9051185
- 546.
Chu B, Zhang A, Huang J, et al. Preparation and biological evaluation of a novel agarose‐grafting‐hyaluronan scaffold for accelerated wound regeneration. Biomed Mater. 2020;15(4):045009.
Not in our library10.1088/1748-605x/ab7b3e
- 547.
Wojcik M, Kazimierczak P, Vivcharenko V, Koziol M, Przekora A. Effect of vitamin C/hydrocortisone immobilization within curdlan‐based wound dressings on in vitro cellular response in context of the management of chronic and burn wounds. Int J Mol Sci. 2021;22(21):11474.
Not in our library10.3390/ijms222111474
- 548.
Tian M, Zhou L, Fan C, et al. Bimetal‐organic framework/GOx‐based hydrogel dressings with antibacterial and inflammatory modulation for wound healing. Acta Biomater. 2023;158:252‐265.
Not in our library10.1016/j.actbio.2022.12.049
- 549.
Zhao H, Huang J, Li Y, et al. ROS‐scavenging hydrogel to promote healing of bacteria infected diabetic wounds. Biomaterials. 2020;258:120286.
Not in our library10.1016/j.biomaterials.2020.120286
- 550.
Luque GC, Moya M, Picchio ML, et al. Polyphenol iongel patches with antimicrobial, antioxidant and anti‐inflammatory properties. Polymers (Basel). 2023;15(5):1076.
Not in our library10.3390/polym15051076
- 551.
Liu C, Wang Y, Wang P, et al. In situ electrospun aloe‐nanofiber membrane for chronic wound healing. Smart Mater Med. 2023;4:514‐521.
Not in our library10.1016/j.smaim.2023.03.003
- 552.
Qian Y, Zheng Y, Jin J, et al. Immunoregulation in diabetic wound repair with a photoenhanced glycyrrhizic acid hydrogel scaffold. Adv Mater. 2022;34(29):e2200521.
Not in our library10.1002/adma.202200521
- 553.
Wang L, Yu Y, Zhao X, et al. A biocompatible self‐powered piezoelectric poly(vinyl alcohol)‐based hydrogel for diabetic wound repair. ACS Appl Mater Interfaces. 2022;14(41):46273‐46289.
Not in our library10.1021/acsami.2c13026
- 554.
Lv H, Zhao M, Li Y, et al. Electrospun chitosan‐polyvinyl alcohol nanofiber dressings loaded with bioactive ursolic acid promoting diabetic wound healing. Nanomaterials (Basel). 2022;12(17):2933.
Not in our library10.3390/nano12172933
- 555.
Zhu W, Dong Y, Xu P, et al. A composite hydrogel containing resveratrol‐laden nanoparticles and platelet‐derived extracellular vesicles promotes wound healing in diabetic mice. Acta Biomater. 2022;154:212‐230.
Not in our library10.1016/j.actbio.2022.10.038
- 556.
Zhong G, Qiu M, Zhang J, et al. Fabrication and characterization of PVA@PLA electrospinning nanofibers embedded with Bletilla striata polysaccharide and Rosmarinic acid to promote wound healing. Int J Biol Macromol. 2023;234:123693.
Not in our library10.1016/j.ijbiomac.2023.123693
- 557.
Zhu M, Chen YZ, Ou JZ, et al. [Effects and mechanism of water‐soluble chitosan hydrogel on infected full‐thickness skin defect wounds in diabetic mice]. Zhonghua Shao Shang Za Zhi. 2022;38(10):923‐931.
Not in our library10.3760/cma.j.cn501225-20220507-00175
- 558.
Singh S, Nwabor OF, Sukri DM, et al. Poly (vinyl alcohol) copolymerized with xanthan gum/hypromellose/sodium carboxymethyl cellulose dermal dressings functionalized with biogenic nanostructured materials for antibacterial and wound healing application. Int J Biol Macromol. 2022;216:235‐250.
Not in our library10.1016/j.ijbiomac.2022.06.172
- 559.
- 560.
Su HY, Yang CY, Ou HT, et al. Cost‐effectiveness of novel macrophage‐regulating treatment for wound healing in patients with diabetic foot ulcers from the Taiwan health care sector perspective. JAMA Netw Open. 2023;6(1):e2250639.
Not in our library10.1001/jamanetworkopen.2022.50639
- 561.
- 562.
- 563.
Liu Y, Hu P, Zheng Z, et al. Photoresponsive vaccine‐like CAR‐M system with high‐efficiency central immune regulation for inflammation‐related depression. Adv Mater. 2022;34(11):e2108525.
Not in our library10.1002/adma.202108525
- 564.
Chocarro L, Blanco E, Fernández‐Rubio L, et al. Cutting‐edge CAR engineering: beyond T cells. Biomedicines. 2022;10(12):3035.
Not in our library10.3390/biomedicines10123035
- 565.
Usui‐Ouchi A, Giles S, Harkins‐Perry S, et al. Integrating human iPSC‐derived macrophage progenitors into retinal organoids to generate a mature retinal microglial niche. Glia. 2023;71(10):2372‐2382.
Not in our library10.1002/glia.24428
- 566.
Li Y, Che J, Chang L, et al. CD47‐ and integrin α4/β1‐comodified‐macrophage‐membrane‐coated nanoparticles enable delivery of colchicine to atherosclerotic plaque. Adv Healthc Mater. 2022;11(4):e2101788.
Not in our library10.1002/adhm.202101788
- 567.
Hou X, Zhang X, Zhao W, et al. Vitamin lipid nanoparticles enable adoptive macrophage transfer for the treatment of multidrug‐resistant bacterial sepsis. Nat Nanotechnol. 2020;15(1):41‐46.
Not in our library10.1038/s41565-019-0600-1
- 568.
Xu L, Sharkey D, Cantley LG. Tubular GM‐CSF promotes late MCP‐1/CCR2‐mediated fibrosis and inflammation after ischemia/reperfusion injury. J Am Soc Nephrol. 2019;30(10):1825‐1840.
Not in our library10.1681/asn.2019010068
- 569.
- 570.
- 571.
Yan D, Liu S, Zhao X, et al. Recombinant human granulocyte macrophage colony stimulating factor in deep second‐degree burn wound healing. Medicine (Baltimore). 2017;96(22):e6881.
Not in our library10.1097/md.0000000000006881
- 572.
Luo B, Sun HT, Wang YT, et al. Clinical efficacy of rhGM‐CSF gel and medical collagen sponge on deep second‐degree burns of infants: a randomized clinical trial. Medicine (Baltimore). 2024;103(1):e36304.
Not in our library10.1097/md.0000000000036304
- 573.
Zhang XH, Cui CL, Zhu HY, et al. The effects of recombinant human granulocyte‐macrophage colony‐stimulating factor gel on third‐degree frostbite wounds in northeastern china: a randomized controlled trial. J Burn Care Res. 2023;44(3):715‐722.
Not in our library10.1093/jbcr/iraa019
- 574.
Wu Y, Shen G, Hao C. Negative pressure wound therapy (NPWT) is superior to conventional moist dressings in wound bed preparation for diabetic foot ulcers: A randomized controlled trial. Saudi Med J. 2023;44(10):1020‐1029.
Not in our library10.15537/smj.2023.44.20230386
- 575.
Wu DC, Kollipara R, Carter MJ, Goldman MP. A novel macrophage‐activating gel improves healing and skin quality after CO2 laser resurfacing of the chest. Dermatol Surg. 2022;48(12):1312‐1316.
Not in our library10.1097/dss.0000000000003622
- 576.
Sanpinit S, Chokpaisarn J, Na‐Phatthalung P, et al. Effectiveness of Ya‐Samarn‐Phlae in diabetic wound healing: evidence from in vitro studies and a multicenter randomized controlled clinical trial. J Ethnopharmacol. 2024;326:117929.
Not in our library10.1016/j.jep.2024.117929
- 577.
Mirastschijski U, Schwab I, Coger V, et al. Lung surfactant accelerates skin wound healing: a translational study with a randomized clinical phase i study. Sci Rep. 2020;10(1):2581.
Not in our library10.1038/s41598-020-59394-5
- 578.
Robinson H, Jarrett P, Vedhara K, et al. The effect of expressive writing on wound healing: Immunohistochemistry analysis of skin tissue two weeks after punch biopsy wounding. J Psychosom Res. 2022;161:110987.
Not in our library10.1016/j.jpsychores.2022.110987
- 579.
Ud‐Din S, Foden P, Mazhari M, et al. A double‐blind, randomized trial shows the role of zonal priming and direct topical application of epigallocatechin‐3‐gallate in the modulation of cutaneous scarring in human skin. J Invest Dermatol. 2019;139(8):1680‐1690. e16.
Not in our library10.1016/j.jid.2019.01.030
- 580.
Ud‐Din S, Wilgus TA, McGeorge DD, Bayat A. Pre‐emptive priming of human skin improves cutaneous scarring and is superior to immediate and delayed topical anti‐scarring treatment post‐wounding: a double‐blind randomised placebo‐controlled clinical trial. Pharmaceutics. 2021;13(4):510.
Not in our library10.3390/pharmaceutics13040510
- 581.
Niebuhr M, Mühlradt PF, Wittmann M, Kapp A, Werfel T. Intracutaneous injection of the macrophage‐activating lipopeptide‐2 (MALP‐2) which accelerates wound healing in mice–a phase I trial in 12 patients. Exp Dermatol. 2008;17(12):1052‐1056.
Not in our library10.1111/j.1600-0625.2008.00750.x
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