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Challenges and strategies for in situ endothelialization and long-term lumen patency of vascular grafts

Yu Zhuang, Chenglong Zhang, Mengjia Cheng and 5 more

Bioactive Materials · 2021 · Review · CC BY

doi:10.1016/j.bioactmat.2020.11.028

Abstract

Vascular diseases are the most prevalent cause of ischemic necrosis of tissue and organ, which even result in dysfunction and death. Vascular regeneration or artificial vascular graft, as the conventional treatment modality, has received keen attentions. However, small-diameter (diameter < 4 mm) vascular grafts have a high risk of thrombosis and intimal hyperplasia (IH), which makes long-term lumen patency challengeable. Endothelial cells (ECs) form the inner endothelium layer, and are crucial for anti-coagulation and thrombogenesis. Thus, promoting in situ endothelialization in vascular graft remodeling takes top priority, which requires recruitment of endothelia progenitor cells (EPCs), migration, adhesion, proliferation and activation of EPCs and ECs. Chemotaxis aimed at ligands on EPC surface can be utilized for EPC homing, while nanofibrous structure, biocompatible surface and cell-capturing molecules on graft surface can be applied for cell adhesion. Moreover, cell orientation can be regulated by topography of scaffold, and cell bioactivity can be modulated by growth factors and therapeutic genes. Additionally, surface modification can also reduce thrombogenesis, and some drug release can inhibit IH. Considering the influence of macrophages on ECs and smooth muscle cells (SMCs), scaffolds loaded with drugs that can promote M2 polarization are alternative strategies. In conclusion, the advanced strategies for enhanced long-term lumen patency of vascular grafts are summarized in this review. Strategies for recruitment of EPCs, adhesion, proliferation and activation of EPCs and ECs, anti-thrombogenesis, anti-IH, and immunomodulation are discussed. Ideal vascular grafts with appropriate surface modification, loading and fabrication strategies are required in further studies.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 24, 2026. Paragraph numbers are ours, so an answer can point at one.

Introduction

Vascular diseases are the most prevalent cause of ischemic necrosis of tissue and organ, which has attracted much attention. Vascular defect caused by trauma or underlying diseases like diabetes can reduce oxygen and nutrients supply for tissues and organs, which may result in severe consequences, like claudication, sores, organ disfunctions, necrosis, or even death. When long-segment defects occurred or the defects happened in vital organs like heart, artificial vascular grafts are required to restore blood supply for tissues.

Synthetic vascular grafts have been widely utilized in clinics as conventional strategies for vascular impairment, like polyurethane, polyester, expanded polytetrafluoroethylene (ePFTE), and etc., with diameter greater than 6 mm. However, these synthetic grafts have long-term risk since they are prone to intimal hyperplasia (IH) and thrombogenesis, and result in implantation failure, particularly for small diameter vascular grafts (diameters less than 4 mm). Hence, ideal vascular grafts are required to imitate the framework and constitution of native vessels, as well as inhibit protein deposition, blood coagulation, and immunological rejection. To construct a biomimetic vascular graft, it is indispensable to figure out the critical factors and challenges in graft development.

It has been widely recognized that endothelialization is critical for blood contacting devices. The endothelium, the inner tunica with monolayer endothelial cells (ECs) lining in vessel lumen, directly contacts with blood, and plays an important role in maintaining vascular hemostasis and patency by releasing regulatory molecules including nitric oxide (NO), heparins, and plasmin, etc.. Losing endothelium layer may lead to a cascade of pathological reactions, like thrombogenesis, inflammation reactions, and smooth muscle cell (SMC) hyperplasia. Thus, endothelium regeneration is crucial for vascular graft.

In conventional tissue engineered vascular grafts (TEVGs), ECs are cultured and seeded on scaffolds prior to implantation, which is called in vitro endothelialization. The proliferation ability of in vitro cultured ECs is limited. And greater stemness stem cells are applied, like endothelial progenitor cell (EPC), induced Pluripotent Stem Cell (iPSC), and mesenchymal stem cell (MSC). However, the viability, bioactivity and stability of seeded cells after implantation cannot guarantee, and the clinical application of this strategy is inhibited by its poor effectiveness and practicality. Moreover, in vitro cell culture consumes more time and cost, and have greater risk of contamination. In situ endothelialization, commanding the regeneration of a healthy endothelium on the surface of vascular grafts directly after implantation, is more effective than in vitro endothelialization. Early strategies pay attention to appealing cells from anastomotic regions, but poor EC proliferative ability hinders the long-term expectation. Thus, the mobilization, recruitment and homing of EPC from peripheral blood and bone marrow has appealed much attentions. Furthermore, ideal in situ endothelialization needs more attention on biomaterial type, surface modification and releasing factors to regulate cell performance, in which enhanced adhesion, orientation, proliferation and activation of ECs and EPCs on graft surface are required.

For long-term patency, thrombogenesis is the key factor leading to vascular occlusion. Vascular grafts, as the foreigner directly exposed to blood flux in vasculature, are easy to cause protein deposition and provoke thrombogenesis. The aggregation of insoluble fibrin, platelet, and red cells induces the coagulation cascades and results in thrombus formation. ECs serve as the first line for thrombogenesis. ECs can release and control key molecules, including tissue plasminogen activator (tPA), anti-thrombins, and plasmin, etc., to modulate anti-thrombogenesis process for vascular grafts, and these molecules are also potential treating drugs for application. Another high potential risk is IH. The platelets, inflammatory cells, and SMCs aggregate and release growth factors, resulting in SMCs proliferating and migrating to vascular intima uncontrolledly, which exerts adverse effects on lumen patency.

Furthermore, inflammatory responses, induced by vascular graft implantation, are crucial in modulating graft development. Biomaterial degradations act as stimulus, activate toll-like receptors (TLRs), and thus induce initial inflammation responses, which then cause white blood cells including neutrophils, monocytes, and lymphocytes to infiltrate from blood flow to implantation scaffolds. And then growth factors released by macrophages, like tumor necrosis factor-α (TNF-α), TNF-β, and interleukin-1 (IL-1), etc., may play a role in influencing the biological behavior of ECs and SMCs, and thus modulating in situ endothelialization and lumen patency of vascular graft.

Maintaining long-term lumen patency for small-diameter vascular graft is still challenging. Days after graft implantation, the proliferation of ECs happens, and simultaneously blood cells, platelets and fibrin deposit onto foreign graft. Weeks after implantation, more ECs proliferate and adhere onto graft surface, but no intact EC layer forms, and coagulation cascades may be activated, then resulting in thrombogenesis. Months after implantation, SMCs migrate from anastomotic sites and proliferate uncontrollably, thus leading to IH. Meanwhile, inflammatory cells, especially macrophages, can regulate EC and SMC behavior via inflammatory factors. The process is shown in Fig. 1.

Multiple strategies can be adopted to respond to the challenges described above for enhanced long-term lumen patency of vascular grafts (Fig. 2). ECs form the inner endothelium layer, and are crucial in preventing coagulation and thrombogenesis. Thus, promoting in situ endothelialization in vascular graft remodeling takes top priority, which requires recruitment of EPCs, migration, adhesion, proliferation and activation of EPCs and ECs. Surface modification with heparin or hydrophilic polymers can reduce thrombogenesis, and some drug release can inhibit IH. Additionally, NO and macrophages also play a crucial role in regulating the biological behavior of ECs and SMCs. Thus, in this paper we will review and summarize different strategies in promoting in situ endothelialization and inhibiting thrombogenesis and IH for long-term lumen patency of vascular grafts.

Homing and adhesion of EPCs and ECs for enhanced in situ endothelialization

EPCs, circulating cells located in bone marrow and low quantities in peripheral blood, can differentiate into ECs. EPCs has also been applied in cell therapy for the treatment of critical limb ischemia. It has been recognized that EPCs plays a critical role in endothelialization of vascular grafts. However, the quantity of EPC homing to the neovascularization sites is limited. For enhanced in situ endothelialization, the homing of EPCs and recruitment of ECs is vital, which includes chemotactic effects, capture and adhesion of cells on graft surface. Multiple chemokines can be utilized for EPC chemotaxis, and strategies like nanofibrous structure, biocompatible surface with bioactive binding sites and specific molecules modification can be applied for cell adhesion (Fig. 3).

Homing of EPCs by chemokines

EPCs have multiple sub-populations and display different markers on their surface. Early EPCs display markers including CD34, CD133 and VEGFR2, etc., which are reduced as cell maturity increases. These EPCs in different subpopulations exert synergistic effects on endothelialization. Multiple chemokines that can be utilized for EPC homing are summarized in Table 1.

The quantity of EPCs in circulation blood flow is low, and EPCs from bone marrow can mobilize into peripheral blood for enhanced endothelialization. Multiple growth factors play a role in the chemotaxis of EPC homing to the region of neovascularization, but the underlying mechanism of signaling pathways in EPC homing has not been elaborated.

Chemokines targeting CXC families on EPC surface

Stromal cell-derived factor-1α (SDF-1α), which can act as the chemoattract for CXC family, has potential in EPCs chemotaxis and recruitment. SDF-1α can bind to CXCR4 on hematopoietic stem cell (HSC) surface for stem cell homing, and it has also been reported that SDF-1α can bind to CXCR4 expressed on EPC surface. Yu et al. immobilized SDF-1α on vascular graft and found that SDF-1α immobilization could recruit EPCs and smooth muscle progenitor cells (SMPCs) simultaneously for enhanced in situ endothelialization. The in vivo results indicated that the lumen patency 12 weeks after implantation for naked graft was 44%, heparin coated graft was 67%, and SDF-1α/heparin modified graft was 89%. Issa et al. studied the performance of dickkopf-3 (Dkk3) and results indicated that Dkk3 could interact with cell surface ligand CXCR7, activate ERK1/2 and PI3K/AKT signaling pathway, and thus enhance the recruitment and differentiation of EPCs.

Chemokines can directly immobilize on graft surface, for example, Wang et al. immobilized SDF-1α onto PLLA/PLGA/PLCL vascular scaffolds for EPC homing. Nanoparticles (NPs) are also ideal strategy for bioactive molecules carrier. He et al. constructed chitosan/fucoidan NPs to load SDF-1α to induce EC migration for promoted in situ endothelialization.

Chemokines targeting integrin families on EPC surface

It has been reported that the integrins play a role in homing of EPCs. De Visscher et al. constructed a synthetic graft coated with fibronectin (FN) and SDF-1α, and proved that FN could activate α4-integrin-VCAM1/FN axis for EPC homing. Particularly, integrinβ2 have potential in regulating EPC recruitment to ischemic sites. Chavakis et al. found that integrinβ2 not only induced the adherence of EPCs to ECs and ECM proteins, but also regulated the chemotaxis of EPCs to the neovascularization sites. Furthermore, integrinβ2 activated by specific anti-β2-integrin antibody can effectively enhance the homing of EPCs for in situ endothelialization. Integrin mediated migration of EPCs can be promoted by enhancing the activity of GTPase Rap1, and Rap1 can be activated by Epac1. Carmona et al. utilized 8-pCPT-2′-O-Me-cAMP to directly activate Rap1 for recruitment of EPCs, providing a new strategy for promoted homing of EPCs..

Moreover, some other molecules have also been explored and found to be able to promote homing of EPCs, like ephrine-B2-Fc chimera and HMGB-1, which target to specific receptors on EPC surface.

The markers like CD34 and CD133 on EPC surface are not specific, which may also display on hematopoietic stem cell (HSC) surface. Lacking specific makers on EPC surface for chemokines reduces homing efficiency. Moreover, the mechanism under chemokines induced stem cell homing has not been clearly figured out. Deep explorations are needed to uncover the mechanism, and more specific chemokines are required to effectively promote homing and recruitment of EPCs for endothelialization.

Adhesion of EPCs and ECs on graft surface

After homing of EPCs, cell adhesion on graft surface utilizing nanofibrous structure, biocompatible surface with bioactive binding sites or specific molecules modification takes prior consideration (Fig. 3).

Biomimetic nanofibrous scaffolds for enhanced cell adhesion

Extracellular matrix (ECM), with nanoscale construction, is the micro-environment for cell adhesion, proliferation and differentiation, and is essential for the maintenance of cell biological activity. Biomimetic nanofibrous scaffolds, with greater surface to volume ratio, provide more binding ligands for cell adhesion and biomolecules adsorption. Multiple approaches can be applied to obtain nanoscale vascular grafts. Generally, there are three approaches for nanofiber fabrication in vascular graft construction, including self-assembly, phase separation, and electrospinning, etc.

Self-assembly is a fabrication process by which individual components are arranged into hierarchical organized structures spontaneously supported by non-covalent interactions. This process is ubiquitous in various molecular bio-behavior. Peptide amphiphiles (PAs) have been widely applied in fabricating collagen-like adaptable nanofibrous biomaterials utilizing self-assembly strategy. Nanofibrous structure developed by self-assembly can simulate the ECM with the lowest scale at 5–8 nm, but the synthesis process is difficult to be regulated and the efficiency of productivity is relatively low. Thus, the application of this strategy in vascular graft construction is limited. Phase separation can also fabricate nanofibers at the size similar to native ECM collagens, with different porous structures at macroscale, which can also effectively enhance cellular adhesion onto the scaffold surfaces. Various biodegradable aliphatic polyesters can be developed into nanofibers using phase separation, with fiber diameter ranging between 50 and 500 nm. The porosity and pore sizes can be tuned by modulating parameters, like polymer concentrations, porogen morphology utilized, gel temperatures and frozen temperatures. Compared to self-assembly strategy, phase separation is a relatively simpler strategy that does not need professional techniques. However, its application is restricted because of low yield efficiency, a finite number of selected polymers for fabrication and consequently inappropriate for industrialized scale manufacture.

Electrospinning has been considered as an appealing strategy to simulate native ECM, for its simplicity and scalability. To fabricate optimal electrospun scaffolds, construction parameters including voltage, solution concentration, interval to collector, and collection approaches, can be tailored to acquire ideal fibrous orientation, diameters, porosity and mechanic characteristics. Compared to self-assembly and phase separation, a broader spectrum of biomaterials can be produced into nanofibers using electrospinning. Furthermore, convenient preparation methods, abundant biomaterials with electrospin-ability and high yield efficiency make the electrospinning strategy accessible for scaffold fabrication both on laboratory and industrial scales.

Multiple biomaterials have been utilized in electrospinning, including synthetic polymers, natural polymers and hybrid biomaterials. Non-degradable synthetic polymers like poly (ethylene terephthalate) (PET), expanded poly (tetrafluoroethene) (ePTFE), polyurethane (PU) have ideal electrospinnability and outstanding mechanical characteristics. Non-degradable biomaterials can be implanted for long term application, but excellent tissue engineered grafts should possess proper biodegradability for minimized inflammatory reactions. Degradable biomaterials are favorable for adhesion and proliferation of ECs. Biodegradable synthetic polymers like poly (ε-caprolactone) (PCL), PGA, PLGA, and natural polymers like collagen, elastin, silk fibroin, gelatin, are also applied for vascular graft fabrication. Natural polymers have ideal biocompatibility, but insufficient mechanical properties. It is an appealing approach to blend the natural polymers possessing outstanding biocompatibility with the synthetic polymers possessing adequate mechanical properties to overcome these disadvantages, for example, collagen and PEG, elastin and PCL, gelatin and PVA, etc. For construction of biomimetic vessel structure, layer by layer (LBL) strategy can be applied in vascular graft fabrication, for example, silk fibroin as inner layer, hydrogels as the medial, and TPU nanofibers as outer layer, to simultaneously obtain mechanical strength and biological activity, and simulate natural vessel structure.

Biocompatible surface with bioactive binding sites for enhanced cell adhesion

Synthetic polymers can provide sufficient mechanical strength in vascular graft construction, but inadequate bioactivity since lacking sufficient cellular recognition sites for cell adhesion. Natural polymers with outstanding biocompatibility can provide enough cellular ligands. Thus, surface modification with natural polymer for synthetic polymers is an effective strategy for enhanced cell adhesion in vascular graft fabrication.

Gelatin possesses cell surface binding ligands RGD which are favorable for cell adhesion. Gelatin has attracted much attention for surface modification because of its biocompatibility, biodegradability, and editability. Cationized gelatin can be covalently grafted on electrospun PLLA nanofibers for better surface bioactivity. Merkle et al. applied co-axial electrospinning to construct core-shell structure, with PVA as core to provide mechanical strength, and with gelatin as shell to display biocompatible surface. The Young's modulus of core-shell structure was about 169 MPa and the tensile strength was about 5.4 MPa, and the mechanical properties was greatly enhanced compared with single PVA or gelatin. Blended gelatin and heparin can also be an alternative strategy. Wang et al. fabricated gelatin, heparin NPs, and polylysine nano-coating using self-assembly to construct a biomimetic vascular structure.

Collagen, component of natural ECM, possesses excellent biocompatibility and bioactivity. Grus et al. fabricated polyester vascular scaffold coated with collagen to enhance biocompatibility and improve lumen long-term patency. Furthermore, vascular graft PolyMaille (Perouse Medical, France) with collagen coating is already available. Some other natural polymers, like elastin, silk fibrin, are also alternative for vascular graft application. These polymeric coatings can provide non-specific binding sites not only for EC adhesion, but also for other blood cells like platelets, white cells, and SMCs, which may induce thrombogenesis and IH. Thus, more specific binding coatings are required for in situ endothelialization.

Cell-capturing molecules on surface for enhanced cell adhesion

EPCs can differentiate into ECs and generate the inner endothelium layer on graft surface. Hence, it is important to targetedly capture the circulating EPCs and ECs onto graft surfaces for enhanced in situ endothelialization. To promote the migration and adhesion of cells, antibodies, cell adhesive peptides and cell-specific aptamers have been extensively investigated.

CD34 and VEGFR-2 are the surface markers on EPC surface. Anti CD34 antibodies (Ab) have been the most widely utilized for EPC target and capture. But there are some disadvantages concerning about anti CD34 Abs, since anti CD34 Abs are not only specific for EPCs, they can also capture other cells, some of which can even differentiate into SMCs and lead to thrombosis. Clinical investigations indicated that anti CD34 Abs coated graft cannot reduce risk of vascular occlusions than conventional graft surface, especially of IH. To overcome this problem, it was proposed that anti CD34 Abs can combine with drugs like sirolimus to reduce IH. Anti VEGFR-2 Abs are also alternative for EPC capture. Anti VEGFR-2 Abs can effectively target and capture EPCs and ECs from blood flowing. It has been reported that the specificity of VEGFR is superior than that of CD34 and CD31. Although the superior specificity, the VEGFR-2 also expresses on surface of monocytes and macrophages, and the recruitment of immune cells will induce undesirable inflammatory responses. The specific markers for stem cell recognition remains unclear and needs more explorations.

Cell adhesive peptides are also critical for biological identification between cell membrane and relevant ligand for cell capture and adherence. Integrins on cell surface mediate the adhesion of cell onto ECM in a dominated manner. Multiple peptide sequences have been applied for surface modification for enhanced adhesion of EPCs and ECs, including RGD, CAG, REDV, and YIGSR, etc. These peptide sequences modified on graft surface display specific affinity with ECs, enhancing the adhesion of ECs and inhibiting the adherence of platelets.

Aptamer, the short oligonucleotide sequences, exhibits affinity to specific targeted molecules. Aptamer sequences can be obtained through cell-SELEX technology. It was reported that aptamer could capture porcine EPCs for enhanced in situ endothelialization. But the application of aptamers in EPC capture has not been widely used. The effects of aptamers on the in vitro and in vivo cell performance and vascular patency still require more studies to verify. The stability of aptamers in vivo is unclear. Moreover, some aptamers have risks of causing inflammation responses, and the relative immunomodulation is poor known.

The cell-adhesive peptides, originating from ECM, bind to integrins on EC surface for cell capture. The ECs possess stronger specificity to peptides like YIGSR and REDV than SMCs. Peptides can promote cell adhesion, but with poor targeting. Antibodies can target to relevant markers on cell surface, but the targeting markers are not specific on EPC or EC surface. Aptamers, the oligonucleotide sequence, have high affinity with target cells. However, the immune responses of aptamers in vivo remain unclear.

Cell behavior regulation for enhanced in situ endothelialization

Ideal vascular graft is also required for enhanced cell elongation, proliferation, activation and differentiation of EPCs and ECs.

Circulating EPCs can be subdivided into two main categories, hematopoietic lineage EPCs and nonhematopoietic lineage EPCs. The hematopoietic EPCs originate from bone marrow and represent a provasculogenic subpopulation of hematopoietic stem cells (HSCs), which play an indispensable role in vascular repair. Different stem cells have different stemness. Embryonic stem cells (ESCs) possess totipotent differentiation potential, and mesenchymal stem cells (MSCs) are also pleuripotent in osteogenic, chondrogenic and adipogenic differentiation. But the stemness and differentiation potential of EPCs, the somatic stem cell, is limited, without multiple differentiation potential. Under normal physiological conditions in adults, the stem cells are in quiescent conditions, and maintain a dynamic balance in growth and decay of tissues. But under pathological conditions or external inductions, the ability to differentiate, regenerate and re-new can be activated. Thus, after the circulating EPCs are recruited, the defected vascular environment will release the molecules, and initiate the oriented differentiation of EPCs into ECs. To further enhance the proliferation and oriented differentiation of EPC to EC for promoted endothelialization, topography to regulate cell orientation, bioactive molecules and therapeutic genes can be applied.

Regulated cell alignment and orientation

Topography cues for vascular graft surface can exert significant effects on modulating biological behaviors of ECs and endothelialization. Micro- and nano-scale topography factors including aligned nanofibers and surface patterns can induce the formation of uniformly aligned ECs for intima construction.

Aligned nanofibers

Electrospinning technology has been widely applied in nanofibrous vascular graft fabrication, and fiber orientation can be tuned by regulating spinning parameters. The aligned nanofibers can induce cell orientation and modulate cell morphologies and biological performances. Multiple studies have reported that the axially oriented fibers can arrange the morphology and alignment of ECs or MSCs for intima reconstruction. Furthermore, the aligned fibers can also provide tensile mechanical strength, enhance SMC alignment in outer layer, and higher lumen patency rate.

Surface micro- and nano-patterns

Cell-surface interactions play a crucial role in enhancing endothelialization. Graft surface with micro-/nano-scale grove/ridge patterns can enhance the construction of an intact EC layer spontaneously aligned along a prior orientation, which then effectively simulates the elongated endothelium layer structure. The aligned ECs have been reported to inhibit leukocyte invasion and consistent with elongated morphology of native ECs under blood flow.

Surface patterning has potential in promoting spontaneous in situ endothelialization. Photolithography, electron beam lithography, and soft lithography can be utilized to develop micro-/nano-scale tube/groove/pillar patterns in different sizes. The patterns can enhance EC elongation and endothelialization, as well as inhibit platelet adhesion and maintain long-term patency rate. Wang et al. constructed a biomimetic vascular graft modified with nano-topographic lamellar structure utilizing freeze-cast technique, and the lamella was 10 μm high, 200 nm thick (Fig. 4A). The results indicated that the nano-lamellar framework could prevent platelet activation and enhance EC orientation (Fig. 4C). The number of platelet adhesion on lamellar surface was about 3 times fewer than that on non-lamellar surface. The HE staining images indicated that lamellar structure could promote in situ endothelialization, while distinct thrombus formed in non-lamellar structure group (Fig. 4D). Zorlutuna et al. constructed a vascular graft with channel nanopatterns at the periodicity of 650 nm. The nanopatterns were on both sides of surface to induce orientation and proliferation of ECs and SMCs simultaneously. Different surface nanopatterns are effective strategies to tune cell orientation and vascular remodeling in a pattern-dependent way.

The arrangements of adhesive peptides also influence the migration, morphology and proliferation of ECs. Wang et al. explored the effects of RGD nano-spacing in different nanoscale size (37–124 nm) on MSC performance, and the results indicated that RGD nano-spacing might have a role in modulating differentiation of MSCs. Saux et al. found that micro-scale pyramids could impede cell migration, while RGD spacing with density of 6✕108 mm2 could enhance cell spreading and adhesion. Karimi et al. compared random and nano-clustered RGD spacing on vascular graft surface, and demonstrated that the nano-island pattern on surface could promote the migration and adhesion of ECs for enhanced in situ endothelialization. RGD is specific for EC capture, and designing RGD pattern on surface can further promote cell migration and proliferation.

Promoted cell proliferation and activation

To promote the proliferation and activation of ECs and EPCs after cell adhesion, bioactive molecules and therapeutic genes are promising approaches (Fig. 5).

Microenvironment regulation for enhanced cell performance

Multiple molecules possess capability to motivate the proliferation, differentiation and activation of ECs and EPCs, including growth factors, gas and microRNAs (Fig. 5). Vascular endothelial growth factor (VEGF) is vital in vascularization, and plays a key role in regulating EC behavior. Sustained VEGF releasing in vascular graft can promote endothelialization via facilitating differentiation of EPCs and enhancing the proliferation and activation of ECs. VEGF can be loaded on vascular grafts through multiple strategies, like NPs, coaxial electrospinning, direct blending electrospinning, and emulsion electrospinning, etc. Remarkably, VEGF can also serve as chemotaxis for EPC homing via target of VEGFR1 and VEGFR2 receptors on cell surface. Fibroblast growth factor-2 (FGF-2), with potential in directing stem cell differentiation, is also applied in vascular graft. Rajangam et al. combined heparin and PAs, and constructed a self-assembly nanofibrous gel to capture VEGFs and FGF-2 for enhanced angiogenesis. Furthermore, platelet-derived growth factor (PDGF) can promote the migration and proliferation of SMCs. Han et al. constructed a double-layer electrospun nanofibrous scaffold, with inner layer loaded with VEGF for EC proliferation, and outer layer with PDGF for SMC proliferation, thus inducing an intact vascular blood vessel formation. Growth factors can directly play a role in vascular construction, but for protein delivery, protein bioactivity and concentration maintenance in vivo are still concerned. To enhance delivery efficiency and maintain protein activity and concentration in vivo, multiple nanoscale and microscale carriers are utilized, which are summarized in Table 2.

VEGF is efficient in promoting proliferation and activation of ECs, but the immunogenicity and high expense make the application of VEGF in clinic difficult. MicroRNAs (miRNAs), the non-coding RNAs, have been reported to play a role in regulating vascularization by bonding with promotor region of target genes in recent studies. It has been showed that miRNA-126 can regulate the vascular development via modulating the responding of ECs to VEGF, and inhibiting Spred-1 expression, which restrains angiogenic signal pathways. Electrospun nanofibers are viable and convenient to load biomolecules, and have been widely utilized to carry miRNAs. Zhou et al. utilized REDV modified PEG-trimethyl chitosan to load miRNA-126, and delivered the miRNA to the targeted ECs. The miRNA complex was incorporated into electrospun polymers utilizing emulsion electrospinning to construct vascular scaffold, and miRNA was released sustainedly for enhanced EC performance. Cui et al. loaded miRNA-126 in inner electrospun fibers, and miRNA-145 in outer fibers, respectively to regulate biological behavior of ECs and SMCs. Moreover, some other miRNAs are also found and explored their effects on vascularization. MiRNA-22 could prevent the apoptosis of SMCs via targeting p38-MAPK pathway during vascular remodeling. Suppression of miRNA-21 restrains EC growing through PTEN dependent-PI3K pathway. Nevertheless, effects of these miRNAs are still at primary research stage, and has not been widely recognized.

Moreover, NO can also stimulate proliferation and activation of ECs, as well as homing of EPCs, which makes NO donors attractive for vascularization. The biological functions and multiple NO donors applied in vascular grafts will be introduced in the following contents.

Therapeutic gene delivery for enhanced cell performance

Delivery of proteins like VEGF and FGF can directly bind to receptors on target cell surface, and modulate the expression of angiogenesis related genes via signaling pathways, but have risk of protein degradation, inactivation and gradual consumption. Gene therapy is a favorable approach for promoting endothelialization through transfecting ECs, since genes can be transfected into nucleus and translated for protein releasing, potential in maintaining a relative high protein concentration in vivo (Fig. 5). VEGF, FGF and ZNF580 genes are promising genes for therapeutic gene delivery in vascular graft applications.

To guarantee the transfection efficiency, gene carriers are vital for delivery. Nanoparticles (NPs) can act as carriers, preventing DNA from degradation by enzymes, targeting to the specific cells, entering cell membrane, translocating to the nucleus, and finally integrating to host genome. Various biomaterials have been widely utilized for gene delivery, including lipid NPs, polymeric NPs like cationic ester polymers, co-polymers, poly (ethylenimine) (PEI), PEI based co-polymers, inorganic NPs like calcium phosphate, and peptide based NPs. Furthermore, electrospinning technology is also attractive in gene loading. Plasmid-DNA (pDNA) can be directly mixed in solvent for electrospinning, or modify nanofibers with gene loaded microparticles.

The cell adhesive peptide like RGD, REDV can be utilized for target gene delivery to facilitate peptide modified pDNA complex bind to integrins on EC surface. Wang et al. constructed a REDV modified pZNF580 NP complexes utilizing self-assembling strategy. The REDV mediated NPs could prevent the pZNF580 from DNase degradation, display better hemocompatibility and enhance delivery efficiency for enhanced in situ endothelialization. Kibria et al. utilized RGD and PEG as dual-ligand modification to promote target gene delivery efficiency.

Delivered genes can integrate into target cell genome, and stably expressing transfected proteins in a long period time, compared with direct protein delivery. But the transfection efficiency is a potential risk, and the transferred genes cannot function in vivo immediately like proteins.

Preventing vascular incidents for long-term lumen patency

Thrombogenesis, IH and calcification can reduce lumen diameter, and are major risks in maintaining long-term lumen patency after vascular implantation. Preventing thrombus formation, IH and calcification is crucial for survival of vascular graft. Hydrophilic surface and heparin coating are effective in anti-thrombogenesis, and some drugs can inhibit IH. Moreover, NO can play a role in inhibiting coagulation and IH.

Anti-thrombogenesis for enhanced long-term lumen patency

It is easy to provoke thrombogenesis if lacking ECs on graft surfaces, but during early healing process, there have not been adequate ECs lining on surface to release molecules for thrombus prevention. Thus, at the beginning of implantation, vascular grafts may direct contact with blood cells in vasculature. The vascular grafts are transplanted as foreign matters, and easy lead to the absorption of plasma proteins and blood cells, and then activate the coagulation cascades. The graft surface with minimized protein adsorption, drugs or gases for anti-coagulation are effective strategies for thrombogenesis prevention.

To inhibit thrombogenesis, minimizing the absorption of plasma proteins on graft surfaces is crucial. Thus, a biocompatible surface with minimized protein adsorption is required. The hydrophilic surface can effectively prevent the protein adsorption. Some biocompatible and hydrophilic biomaterials have been utilized for the surface modification of vascular grafts, for example, PEG, zwitterionic polymers. PEG and zwitterionic polymers or groups can be directly coated, blended or covalently grafted on the scaffold surfaces, and the hydrophilic surfaces can effectively inhibit the protein adsorption and platelet adherence.

Furthermore, heparin, known as an anti-coagulative drug, can be coated or immobilized on vascular graft surface, which plays a role in anti-thrombogenesis. Heparin can interact with anti-thrombase AT III, to restrain the function of thrombase and coagulation factor Xa. Heparin, with carboxyl groups, can also be blended with gelatin to provide a biocompatible and anti-coagulative surface. Liu et al. constructed heparin/poly-l-lysine mixed NPs, and immobilized these NPs on a dopamine modified surface. They found that heparin modified surface could enhance biocompatibility, inhibit fibrin induced platelet adherence, and prolong thrombin time (TT) to 23.7–27.9s. Moreover, LBL technology can be utilized to graft heparin on the graft surfaces. Easton et al. constructed a LBL coating, utilizing ploy (acrylic acid) and polyethyleneimine to immobilized heparin on an electrospun nanofibrous scaffold, and the results indicated that the hemocompatibility of scaffold was enhanced.

Some other anti-coagulation drugs can also be utilized, for example, clopidogrel, warfarin, t-PA. The t-PA is the enzyme converting plasminogen to plasmin, inducing the fibrinolytic process. Liu et al. immobilized t-PA on electrospun PVA nanofibrous mats, aiming to mimic natural fibrinolysis function and prevent thrombus formation. Furthermore, Gastrodin, which is applied in cardiovascular diseases, can lower blood viscosity and regulate inflammation reactions. Zheng et al. fabricated Gastrodin-loaded PU scaffolds, and found that the Gastrodin modified grafts showed greater potential in preventing thrombogenesis and inflammations.

Apart from surface modification and drugs, one novel nanocomposite has been indicated to possess the ability to prevent thrombogenesis and display ideal mechanical characteristics. To inhibit thrombogenesis of PU vascular graft scaffolds and improve bistability of PU in vivo, Kannan et al. attached polyhedral oligomeric silsesquioxane (POSS) nanoparticles into poly (carbonate urethane) (PCU) scaffold with covalent bonding and developed a new POSS-PCU nanocomposite biomaterial. This POSS-PCU nanocomposite can be developed into small-diameter vascular grafts with enhanced mechanical properties and hemocompatibility, free from adverse events like IH and calcification.

For hydrophilic surface, it can reduce fibrin adherence and coagulation cascades, but can also decrease EC adhesion. For heparin modification, the bioactivity and coating density are concerned. Hence, more studies are required to obtain ideal graft surface with reduced platelet and fibrin adherence and enhanced EC adhesion.

Anti-IH for enhanced long-term lumen patency

IH has high incidence in causing long-term vascular occlusion several months after implantation, which is caused by uncontrollable SMC pathological proliferation.ECs, serving as the paramount defender in vascularization, can release molecules for IH inhibition. Apart from promoting EC adhesion and activation, some drugs like E2F and MK2i also have potential in preventing IH by controlling SMC proliferation in a more direct way. In clinic, E2F transcription factor was utilized to keep a 30 min lumen patency for the vascular tissue in vitro. But the clinical trial results indicated that E2F treated grafts in vitro failed to preventing IH via inhibiting proliferation of SMCs after implantation. The p38 MAPK signaling pathway can play a role in activating proliferation of SMCs, and then induce the downstream inflammatory and fibrotic cascades in IH. To prevent IH, Evans et al. utilized MAKP inhibitory peptide (MK2i) and constructed MK2i NPs for graft modification to prevent uncontrollable proliferation of SMCs.

Role of NO in enhancing long-term lumen patency

NO can play an important protective role in vasculature, and also play an effective role in influencing relevant physiological functions (Fig. 6A). In physiological environment, NO is secreted by endothelial cells, which is synthesized through catalytic reactions in the presence of nitric oxide synthase (NOS). NO can inhibit the aggregation and activation of platelets, to avoid thrombogenesis, restrain proliferation of SMCs, to avoid IH, as well as prohibit the recruitment and activation of inflammatory cells, to avoid inflammation (Fig. 6A). Furthermore, NO plays a critical role in promoting the growth of endothelial cells (Fig. 6A). Insufficient ECs lead to deficient NO release, which may then trigger pathological process. Hence, abundant NO release is required to enhance ECs growth, inhibit SMCs proliferation, and provide an appropriate environment for endothelialization of vascular graft.

N-diazeniumdiolates (NONOates) and S-nitrosothiol (RSNOs) can serve as the potential NO donors to be applied in biomaterials. One mole of NONOate [−N(O) = NO−] can be catalyzed to release 2 mol NO via the hydrolysis reactions in the physiological environment (temperature at 37 °C, pH at 7.4). In RSNOs, thiols (-SH) can react with nitrous acid (HNO2) to release NO, generally under the catalysis of copper ion (Cu2+). Selenocystamine (SeCA), having glutathione peroxidase (GPX)-like functions, is also a potential catalysts for NO synthesis by decomposition of RSNOs.

Multiple strategies have been utilized in vascular devices to catalyze NO generation, like selenocystamine (SeCA), metal-phenolic surface, and copper ion (Cu2+). Qiu et al. utilized SeCA coating to catalyze NO generation, and the results indicated that NO can promote EC proliferation and inhibit SMC growth (Fig. 6B and C). The amount of ECs on SeCA/heparin surface was about 1.5–2.0 folds more than that on naked surface, and EC migration distance and density was enhanced by 26% and 23%, respectively on SeCA/heparin compared with the naked one. Nanoparticles (NPs) can serve as effective delivery vehicles for NO release. The better surface to volume rate can offer more chance for optimized quantity of NO donors. Targeted NPs can deliver NO via altering surface chemical characteristic to regulate the localized areas. Various NPs have been studied to serve as carriers for NO donors, including silica nanoparticles (SiNPs), liposome nanoparticles, and metallic nanoparticles.

SiNPs are easily compounded in the nanoscale, and contain functional groups like amine groups (-NH2) on the surface. The amine-functionalized SiNPs were synthesized, with the size ranging from 20 to 500 nm, to serve as NO carriers via converting the –NH2 groups into NONOates donors under high pressure of NO. To promote the storage and releasing characteristics of NO, the synthesis of SiNPs following the preparation of NONOates modified aminosilanes was proposed by the same team. Fumed silica (FS) particles can also serve as NO carrier, and can be embedded into polymers to control NO releasing. Zhang et al. synthesized FS particles (200–300 nm), with NONOates formed on the surface, and embedded within PU films as anti-thrombotic coating.

Liposomes are competent carriers, owing to their efficient cell encapsulation ability. The influence of hydrophobic liposomes and surface micelles on the NO releasing were studied. Dinh et al. found that anionic 1,2-dipalmitoyl-sn-glycero-3-[phospho-(1-glycerol)] sodium salt (DPPG) liposomes possessed greater NO releasing catalysis efficiency than sodium dodecylsulfate (SDS) micelles. Dinh et al. further explored the influence of unilamellar (anionic and cationic) phospholipid vesicles on dissociating NO from NONOates, and found that anionic liposome NPs showed an enhanced NO releasing. Thermosensitive liposome NPs and photo-sensitive NO donors were also explored.

Silica and liposome NPs described above can effectively load and liberate NO, but cannot deliver the gas to targeted tissues. Some metallic NPs are potential strategies to serve as loading vehicles for NO delivery to targeted tissues, including gold (Au) NPs, platinum (Pt) NP, silver (Ag) NPs. Furthermore, metal organic frameworks (MOFs), composed of metal ions as nodes and organic ligands as linkers, have been utilized to embed and release NO to promote re-endothelialization for vascular grafts. Fan et al. constructed nanoscale copper-based MOFs (Cu-MOFs), and proved that Cu-MOFs performed as heterogeneous catalysts for NO regeneration synthesized by endogenous RSNOs. Simultaneous delivery of NO and Cu2+ could restrain restenosis and enhance endothelialization synergistically.

Moreover, NO gas can be combined with growth factor VEGF, and spontaneously released to promote endothelialization and inhibit thrombogenesis and IH. Although multiple studies have proved the influence of NO in in vitro and in vivo experiments, no clinical trials in therapeutic effects of NO donors have been conducted. Furthermore, the therapeutic effects on diabetic wounds still need more concerns.

Immunomodulation in vascular graft development

Inflammatory responses, induced by graft implantation, are crucial in modulating graft development. Molecules released from immune cells influence the biological behavior of ECs and SMCs, and thus modulating in situ endothelialization and lumen patency of vascular graft.

Immunomodulation and in situ endothelialization

Macrophages, as the key cells in innate immunity, can release multiple molecules modulating in situ endothelialization process. It has been reported that TNF-α secreted by macrophages plays a role in regulating migration and differentiation of EPCs and graft development. TNF-α can induce the differentiation of EPCs through activating TNF-α receptor 1 and NF-κB signaling pathway. Moreover, TNF-β1 can promote platelet mediated-EPC homing via integrin β3 on cell surface.

The polarization of macrophages can be controlled to regulate the inflammatory microenvironment. Classical macrophages (M1) may secret inflammation cytokines, while alternatively induced macrophages (M2) tend to activate anti-inflammation molecules and enhance tissue repairment. The acute inflammation responses can be modulated by lipid mediators which possess potential in anti-inflammation, like Resolvins. Shi et al. incorporated Aspirin-Triggered resolvin D1 (AT-RvD1) into electrospun PCL vascular graft, and demonstrated that the incorporation of AT-RvD1 enhanced vessel tube formation in vitro through M2 macrophage polarization.

Inflammatory cells paly a complex role in regulating angiogenesis. VEGF-A is an important modulator in vascularization, and recently one subset type of neutrophils (which was shown as CD49d+VEGFR1highCXCR4high) were identified. Massena et al. demonstrated that homing this subset neutrophils to hypoxia neovascularization site could promote angiogenesis. The interaction between angiogenic cells and inflammatory cells is still not completely clarified, which requires more further explorations.

Immunomodulation and long-term lumen patency

Inflammatory cells also play a role in modulating the long-term lumen patency after graft implantation, like IH and intima calcification. Molecules secreted by macrophages and platelets, like TGF-β, cause enhanced migration and proliferation of SMC, and the unregulated SMC proliferation and the inrush of macrophages are dominating factor leading to IH. SMCs from anastomosed sites migrate towards intima, and SMCs transform from the quiescent phenotype into the dedifferentiated, proliferative type, thus resulting in IH.

Macrophages are the predominant inflammatory cells targeting SMCs, and lead to the pathological proliferation of SMCs. Thus, reducing IH via regulating macrophage behavior has attracted great attention. To attenuate chronic inflammation induced IH, Ding et al. constructed resveratrol (RSV) modified carbon nanotube (CNT) coating for tissue engineered blood vessels. RSV has been reported to inhibit inflammation process via inducing M2 macrophage polarization. The RSV modified CNT can be utilized for macrophage intake, and released intracellularly, which effectively promoted transformation of M1 into M2 and prevented IH. Yang et al. modified a decellularized vascular graft with the rapamycin (RM)-blended electrospun PCL coating, and the results indicated that the RM-loaded graft could enhance M2 polarization, inhibit IH, and promote endothelialization.

Inflammation is also the leading factor contributing to atherosclerotic calcification. Wei et al. extracted small extracellular vesicles (sEVs) containing VEGF, miRNA126, and miRNA145 from MSC, and loaded sEVs on a heparinized electrospun PCL scaffold. Wei et al. found that sEVs loaded graft exhibited immunomodulatory function, and induced the transition of M1 into M2, which effectively reduced graft calcification and enhance lumen patency for hyperlipidemia patients.

Macrophages, the key cell in innate immune system, can polarize from M1 type to M2 type, which is induced by biomaterials, drugs or sEVs, to regulate behavior of ECs and SMCs, thus promote endothelialization and inhibit IH and calcification (Fig. 7). NK cells also play a role in vascular remodeling. BALB/c mice lack in NK functions display distinctly less IH occurrence, but approaches to regulate NK cell functions using bioactive scaffolds have not been available. Generally, the role of complements and cytokines in innate immune system are understood. However, the performance of adaptive immune system, including T cells, B cells and mast cells, is not that clear. For better modulation of immune functions, more studies on regulation of adaptive immune cell behavior are required.

Conclusions and further perspectives

The challenges for in situ endothelailization and long-term patency of small-diameter vascular grafts still exist. ECs form the inner endothelium layer, which play a crucial role in maintaining vascular hemostasis and lumen patency, but homing and capture of EPCs and ECs for conventional graft is poor. Naked graft surface without lined EC layer is easy to be deposited with blood cells, fibronectin, and platelets, thus inducing coagulation cascades and thrombogenesis. Furthermore, uncontrollable proliferation of SMCs migrating to intimal layer may result in IH, and inflammatory cells also play a role in regulating biological behavior of ECs, EPCs, and SMCs.

Multiple strategies can be adopted for enhanced in situ endothelialization and long-term patency of vascular grafts (Fig. 8). Strategies for in situ endothelialization promotion, thrombogenesis and IH prevention, and immunomodulation in vascular graft remodeling are summarized as following.Strategies for enhanced in situ endothelialization:Homing of EPCs: Chemokines aimed at ligands like CXC family and integrin family on EPC surface can be utilized for EPC homing.Migration and adhesion of EPCs and ECs: Nanofibrous structure, biocompatible surface for more binding sites like gelatin and cell-capturing molecules on graft surface including antibodies, specific peptides and aptamers can be applied for better cell adhesion.Proliferation and activation of EPCs and ECs: Topography of scaffold can regulate cell orientation, like aligned nanofibers, surface micro-/nano-patterns, and RGD patterns on surface. Growth factors, microRNAs and therapeutic genes can modulate cell bioactivity.Strategies for long-term patency:Preventing thrombogenesis: Surface modification with heparin or hydrophilic polymers can inhibit activation and adhesion of platelets, as well as activate AT III, thus reduce thrombogenesis.Preventing IH: Some drugs releasing like MK2i can inhibit IH via inhibiting proliferation of SMCs.The role of NO: NO also plays a crucial role in vascular graft remodeling. NO is potential in inhibiting activation of thrombin, platelets, immune cells and proliferation of SMCs, as well as promoting proliferation and activation of ECs.Strategies for modulating immunomodulation:

Strategies for enhanced in situ endothelialization:

Homing of EPCs: Chemokines aimed at ligands like CXC family and integrin family on EPC surface can be utilized for EPC homing.

Migration and adhesion of EPCs and ECs: Nanofibrous structure, biocompatible surface for more binding sites like gelatin and cell-capturing molecules on graft surface including antibodies, specific peptides and aptamers can be applied for better cell adhesion.

Proliferation and activation of EPCs and ECs: Topography of scaffold can regulate cell orientation, like aligned nanofibers, surface micro-/nano-patterns, and RGD patterns on surface. Growth factors, microRNAs and therapeutic genes can modulate cell bioactivity.

Strategies for long-term patency:

Preventing thrombogenesis: Surface modification with heparin or hydrophilic polymers can inhibit activation and adhesion of platelets, as well as activate AT III, thus reduce thrombogenesis.

Preventing IH: Some drugs releasing like MK2i can inhibit IH via inhibiting proliferation of SMCs.

The role of NO: NO also plays a crucial role in vascular graft remodeling. NO is potential in inhibiting activation of thrombin, platelets, immune cells and proliferation of SMCs, as well as promoting proliferation and activation of ECs.

Strategies for modulating immunomodulation:

Immunomodulation: Some drugs like AT-RvD1, RSV and RM promote M2 polarization, and exert influences on behavior of ECs and SMCs. sEVs can be utilized for M2 polarization and prevent calcification.

Multiple strategies have been explored to promote in situ endothelialization, inhibit thrombogenesis and IH, but the approaches are limited to experimental researches. More researches concerning toxicity, mechanical properties, degradation rate and delivery efficiency should be considered and conducted for further application in clinics.

Author contributions

Y.Z., C.Z., and M.C. collected references, summarized perspectives and wrote the manuscript. J.H. and Q.L. collected references. G.Y. gave the suggestion and help on the revision of this review. K.L. and Y.H. conceived the concept of this review. All authors discussed and commented on the manuscript.

Declaration of competing interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

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    Yu J., Wang A., Tang Z., Henry J., Li-Ping Lee B., Zhu Y., Yuan F., Huang F., Li S. The effect of stromal cell-derived factor-1α/heparin coating of biodegradable vascular grafts on the recruitment of both endothelial and smooth muscle progenitor cells for accelerated regeneration. Biomaterials. 2012;33(32):8062-8074.

    Not in our library10.1016/j.biomaterials.2012.07.042

  52. 52.

    Issa Bhaloo S., Wu Y., Le Bras A., Yu B., Gu W., Xie Y., Deng J., Wang Z., Zhang Z., Kong D., Hu Y., Qu A., Zhao Q., Xu Q. Binding of dickkopf-3 to CXCR7 enhances vascular progenitor cell migration and degradable graft regeneration. Circ. Res. 2018;123(4):451-466.

    Not in our library10.1161/circresaha.118.312945

  53. 53.

    Wang W., Liu D., Li D., Du H., Zhang J., You Z., Li M., He C. Nanofibrous vascular scaffold prepared from miscible polymer blend with heparin/stromal cell-derived factor-1 alpha for enhancing anticoagulation and endothelialization. Colloids Surf. B Biointerfaces. 2019;181:963-972.

    Not in our library10.1016/j.colsurfb.2019.06.065

  54. 54.

    He D., Zhao A.-S., Su H., Zhang Y., Wang Y.-N., Luo D., Gao Y., Li J.-A., Yang P. An injectable scaffold based on temperature-responsive hydrogel and factor-loaded nanoparticles for application in vascularization in tissue engineering. J. Biomed. Mater. Res. 2019;107(10):2123-2134.

    Not in our library10.1002/jbm.a.36723

  55. 55.

    Chavakis E., Aicher A., Heeschen C., Sasaki K., Kaiser R., El Makhfi N., Urbich C., Peters T., Scharffetter-Kochanek K., Zeiher A.M., Chavakis T., Dimmeler S. Role of beta2-integrins for homing and neovascularization capacity of endothelial progenitor cells. J. Exp. Med. 2005;201(1):63-72.

    Not in our library10.1084/jem.20041402

  56. 56.

    Wu Y., Ip J.E., Huang J., Zhang L., Matsushita K., Liew C.C., Pratt R.E., Dzau V.J. Essential role of ICAM-1/CD18 in mediating EPC recruitment, angiogenesis, and repair to the infarcted myocardium. Circ. Res. 2006;99(3):315-322.

    Not in our library10.1161/01.res.0000235986.35957.a3

  57. 57.

    Bos J.L. Epac proteins: multi-purpose cAMP targets. Trends Biochem. Sci. 2006;31(12):680-686.

    Not in our library10.1016/j.tibs.2006.10.002

  58. 58.

    Enserink J.M., Price L.S., Methi T., Mahic M., Sonnenberg A., Bos J.L., Taskén K. The cAMP-Epac-Rap1 pathway regulates cell spreading and cell adhesion to laminin-5 through the alpha3beta1 integrin but not the alpha6beta4 integrin. J. Biol. Chem. 2004;279(43):44889-44896.

    Not in our library10.1074/jbc.m404599200

  59. 59.

    Carmona G., Chavakis E., Koehl U., Zeiher A.M., Dimmeler S. Activation of Epac stimulates integrin-dependent homing of progenitor cells. Blood. 2008;111(5):2640-2646.

    Not in our library10.1182/blood-2007-04-086231

  60. 60.

    Chavakis E., Hain A., Vinci M., Carmona G., Bianchi M.E., Vajkoczy P., Zeiher A.M., Chavakis T., Dimmeler S. High-mobility group box 1 activates integrin-dependent homing of endothelial progenitor cells. Circ. Res. 2007;100(2):204-212.

    Not in our library10.1161/01.res.0000257774.55970.f4

  61. 61.

    Singh N.K., Janjanam J., Rao G.N. p115 RhoGEF activates the Rac1 GTPase signaling cascade in MCP1 chemokine-induced vascular smooth muscle cell migration and proliferation. J. Biol. Chem. 2017;292(34):14080-14091.

    Not in our library10.1074/jbc.m117.777896

  62. 62.

    Foubert P., Silvestre J.-S., Souttou B., Barateau V., Martin C., Ebrahimian T.G., Leré-Déan C., Contreres J.O., Sulpice E., Levy B.I., Plouët J., Tobelem G., Le Ricousse-Roussanne S. PSGL-1–mediated activation of EphB4 increases the proangiogenic potential of endothelial progenitor cells. J. Clin. Invest. 2007;117(6):1527-1537.

    Not in our library10.1172/jci28338

  63. 63.

    Zhao C., Lin K., Wang X. Maintenance and modulation of stem cells stemness based on biomaterial designing via chemical and physical signals. Applied Materials Today. 2020;19.

    Not in our library10.1016/j.apmt.2020.100614

  64. 64.

    Nikolova M.P., Chavali M.S. Recent advances in biomaterials for 3D scaffolds: a review. Bioactive Materials. 2019;4:271-292.

    Not in our library10.1016/j.bioactmat.2019.10.005

  65. 65.

    Jhala D., Rather H., Kedaria D., Shah J., Singh S., Vasita R. Biomimetic polycaprolactone-chitosan nanofibrous substrate influenced cell cycle and ECM secretion affect cellular uptake of nanoclusters. Bioactive Materials. 2019;4:79-86.

    Not in our library10.1016/j.bioactmat.2018.12.004

  66. 66.

    Zhuang Y., Lin K., Yu H. Advance of nano-composite electrospun fibers in periodontal regeneration. Front Chem. 2019;7(495).

    Not in our library10.3389/fchem.2019.00495

  67. 67.

    Stevens M.M., George J.H. Exploring and engineering the cell surface interface. Science. 2005;310(5751):1135-1138.

    Not in our library10.1126/science.1106587

  68. 68.

    Chen J., Zou X. Self-assemble peptide biomaterials and their biomedical applications. Bioactive Materials. 2019;4:120-131.

    Not in our library10.1016/j.bioactmat.2019.01.002

  69. 69.

    De Santis E., Ryadnov M.G. Peptide self-assembly for nanomaterials: the old new kid on the block. Chem. Soc. Rev. 2015;44(22):8288-8300.

    Not in our library10.1039/c5cs00470e

  70. 70.

    Barnes C.P., Sell S.A., Boland E.D., Simpson D.G., Bowlin G.L. Nanofiber technology: designing the next generation of tissue engineering scaffolds. Adv. Drug Deliv. Rev. 2007;59(14):1413-1433.

    Not in our library10.1016/j.addr.2007.04.022

  71. 71.

    Cui H., Webber M.J., Stupp S.I. Self-assembly of peptide amphiphiles: from molecules to nanostructures to biomaterials. Biopolymers. 2010;94(1):1-18.

    Not in our library10.1002/bip.21328

  72. 72.

    Ma Z., Kotaki M., Inai R., Ramakrishna S. Potential of nanofiber matrix as tissue-engineering scaffolds. Tissue Eng. 2005;11(1–2):101-109.

    Not in our library10.1089/ten.2005.11.101

  73. 73.

    Smith L.A., Ma P.X. Nano-fibrous scaffolds for tissue engineering. Colloids Surf. B Biointerfaces. 2004;39(3):125-131.

    Not in our library10.1016/j.colsurfb.2003.12.004

  74. 74.

    Stankus J.J., Soletti L., Fujimoto K., Hong Y., Vorp D.A., Wagner W.R. Fabrication of cell microintegrated blood vessel constructs through electrohydrodynamic atomization. Biomaterials. 2007;28(17):2738-2746.

    Not in our library10.1016/j.biomaterials.2007.02.012

  75. 75.

    Jayaraman K., Kotaki M., Zhang Y., Mo X., Ramakrishna S. Recent advances in polymer nanofibers. J. Nanosci. Nanotechnol. 2004;4(1–2):52-65.

    Not in our library

  76. 76.

    Chen V.J., Ma P.X. Nano-fibrous poly(L-lactic acid) scaffolds with interconnected spherical macropores. Biomaterials. 2004;25(11):2065-2073.

    Not in our library10.1016/j.biomaterials.2003.08.058

  77. 77.

    Hasan A., Memic A., Annabi N., Hossain M., Paul A., Dokmeci M.R., Dehghani F., Khademhosseini A. Electrospun scaffolds for tissue engineering of vascular grafts. Acta Biomater. 2014;10(1):11-25.

    Not in our library10.1016/j.actbio.2013.08.022

  78. 78.

    Thompson C.J., Chase G.G., Yarin A.L., Reneker D.H. Effects of parameters on nanofiber diameter determined from electrospinning model. Polymer. 2007;48(23):6913-6922.

    Not in our library10.1016/j.polymer.2007.09.017

  79. 79.

    Rnjak-Kovacina J., Weiss A.S. Increasing the pore size of electrospun scaffolds. Tissue Eng. B Rev. 2011;17(5):365-372.

    Not in our library10.1089/ten.teb.2011.0235

  80. 80.

    Arras M.M., Grasl C., Bergmeister H., Schima H. Electrospinning of aligned fibers with adjustable orientation using auxiliary electrodes. Sci. Technol. Adv. Mater. 2012;13(3).

    Not in our library10.1088/1468-6996/13/3/035008

  81. 81.

    Venkatraman S., Boey F., Lao L.L. Implanted cardiovascular polymers: natural, synthetic and bio-inspired. Prog. Polym. Sci. 2008;33(9):853-874.

    Not in our library10.1016/j.progpolymsci.2008.07.001

  82. 82.

    Ma Z., Kotaki M., Yong T., He W., Ramakrishna S. Surface engineering of electrospun polyethylene terephthalate (PET) nanofibers towards development of a new material for blood vessel engineering. Biomaterials. 2005;26(15):2527-2536.

    Not in our library10.1016/j.biomaterials.2004.07.026

  83. 83.

    Burrows M.C., Zamarion V.M., Filippin-Monteiro F.B., Schuck D.C., Toma H.E., Campa A., Garcia C.R.S., Catalani L.H. Hybrid scaffolds built from PET and collagen as a model for vascular graft architecture. Macromol. Biosci. 2012;12(12):1660-1670.

    Not in our library10.1002/mabi.201200154

  84. 84.

    Takagi H., Goto S-n, Matsui M., Manabe H., Umemoto T. A contemporary meta-analysis of Dacron versus polytetrafluoroethylene grafts for femoropopliteal bypass grafting. J. Vasc. Surg. 2010;52(1):232-236.

    Not in our library10.1016/j.jvs.2010.02.010

  85. 85.

    Barshes N.R., Ozaki C.K., Kougias P., Belkin M. A cost-effectiveness analysis of infrainguinal bypass in the absence of great saphenous vein conduit. J. Vasc. Surg. 2013;57(6):1466-1470.

    Not in our library10.1016/j.jvs.2012.11.115

  86. 86.

    Williams S.K., Kleinert L.B., Patula-Steinbrenner V. Accelerated neovascularization and endothelialization of vascular grafts promoted by covalently bound laminin type 1. J. Biomed. Mater. Res. 2011;99A(1):67-73.

    Not in our library10.1002/jbm.a.33138

  87. 87.

    Cho Y.K., Park D., Kim H., Lee H., Park H., Kim H.J., Jung D. Bioactive surface modifications on inner walls of poly-tetra-fluoro-ethylene tubes using dielectric barrier discharge. Appl. Surf. Sci. 2014;296:79-85.

    Not in our library10.1016/j.apsusc.2014.01.048

  88. 88.

    Wang H., Feng Y., Behl M., Lendlein A., Zhao H., Xiao R., Lu J., Zhang L., Guo J. Hemocompatible polyurethane/gelatin-heparin nanofibrous scaffolds formed by a bi-layer electrospinning technique as potential artificial blood vessels. Front. Chem. Sci. Eng. 2011;5(3):392-400.

    Not in our library10.1007/s11705-011-1202-0

  89. 89.

    Feng Y., Meng F., Xiao R., Zhao H., Guo J. Electrospinning of polycarbonate urethane biomaterials. Front. Chem. Sci. Eng. 2011;5(1):11-18.

    Not in our library10.1007/s11705-010-1011-x

  90. 90.

    Ye X., Lu L., Kolewe M.E., Park H., Larson B.L., Kim E.S., Freed L.E. A biodegradable microvessel scaffold as a framework to enable vascular support of engineered tissues. Biomaterials. 2013;34(38):10007-10015.

    Not in our library10.1016/j.biomaterials.2013.09.039

  91. 91.

    Kong X., Han B., Li H., Liang Y., Shao K., Liu W. New biodegradable small-diameter artificial vascular prosthesis: a feasibility study. J. Biomed. Mater. Res. 2012;100A(6):1494-1504.

    Not in our library10.1002/jbm.a.33298

  92. 92.

    Rahmati Nejad M., Yousefzadeh M., Solouk A. Electrospun PET/PCL small diameter nanofibrous conduit for biomedical application. Mater. Sci. Eng. C. 2020;110.

    Not in our library10.1016/j.msec.2020.110692

  93. 93.

    Wu H., Fan J., Chu C.-C., Wu J. Electrospinning of small diameter 3-D nanofibrous tubular scaffolds with controllable nanofiber orientations for vascular grafts. J. Mater. Sci. Mater. Med. 2010;21(12):3207-3215.

    Not in our library10.1007/s10856-010-4164-8

  94. 94.

    Iwasaki K., Kojima K., Kodama S., Paz A.C., Chambers M., Umezu M., Vacanti C.A. Bioengineered three-layered robust and elastic artery using hemodynamically-equivalent pulsatile bioreactor. Circulation. 2008;118(14 Suppl):S52-S57.

    Not in our library10.1161/circulationaha.107.757369

  95. 95.

    Iwasaki Y., Sawada S-i, Ishihara K., Khang G., Lee H.B. Reduction of surface-induced inflammatory reaction on PLGA/MPC polymer blend. Biomaterials. 2002;23(18):3897-3903.

    Not in our library10.1016/s0142-9612(02)00135-7

  96. 96.

    Munoz-Pinto D.J., Jimenez-Vergara A.C., Gharat T.P., Hahn M.S. Characterization of sequential collagen-poly(ethylene glycol) diacrylate interpenetrating networks and initial assessment of their potential for vascular tissue engineering. Biomaterials. 2015;40:32-42.

    Not in our library10.1016/j.biomaterials.2014.10.051

  97. 97.

    Zhang F., Xie Y., Celik H., Akkus O., Bernacki S.H., King M.W. Engineering small-caliber vascular grafts from collagen filaments and nanofibers with comparable mechanical properties to native vessels. Biofabrication. 2019;11(3).

    Not in our library10.1088/1758-5090/ab15ce

  98. 98.

    Wise S.G., Byrom M.J., Waterhouse A., Bannon P.G., Ng M.K.C., Weiss A.S. A multilayered synthetic human elastin/polycaprolactone hybrid vascular graft with tailored mechanical properties. Acta Biomater. 2011;7(1):295-303.

    Not in our library10.1016/j.actbio.2010.07.022

  99. 99.

    Elahi M.F., Guan G., Wang L., Zhao X., Wang F., King M.W. Surface modification of silk fibroin fabric using layer-by-layer polyelectrolyte deposition and heparin immobilization for small-diameter vascular prostheses. Langmuir. 2015;31(8):2517-2526.

    Not in our library10.1021/la504503w

  100. 100.

    Merkle V.M., Martin D., Hutchinson M., Tran P.L., Behrens A., Hossainy S., Sheriff J., Bluestein D., Wu X., Slepian M.J. Hemocompatibility of poly(vinyl alcohol)–gelatin core–shell electrospun nanofibers: a scaffold for modulating platelet deposition and activation. ACS Appl. Mater. Interfaces. 2015;7(15):8302-8312.

    Not in our library10.1021/acsami.5b01671

  101. 101.

    Mi H.-Y., Jiang Y., Jing X., Enriquez E., Li H., Li Q., Turng L.-S. Fabrication of triple-layered vascular grafts composed of silk fibers, polyacrylamide hydrogel, and polyurethane nanofibers with biomimetic mechanical properties. Mater. Sci. Eng. C. 2019;98:241-249.

    Not in our library10.1016/j.msec.2018.12.126

  102. 102.

    Tan X., Gao P., Li Y., Qi P., Liu J., Shen R., Wang L., Huang N., Xiong K., Tian W., Tu Q. Poly-dopamine, poly-levodopa, and poly-norepinephrine coatings: comparison of physico-chemical and biological properties with focus on the application for blood-contacting devices. Bioactive Materials. 2021;6(1):285-296.

    Not in our library10.1016/j.bioactmat.2020.06.024

  103. 103.

    Ren X., Feng Y., Guo J., Wang H., Li Q., Yang J., Hao X., Lv J., Ma N., Li W. Surface modification and endothelialization of biomaterials as potential scaffolds for vascular tissue engineering applications. Chem. Soc. Rev. 2015;44(15):5680-5742.

    Not in our library10.1039/c4cs00483c

  104. 104.

    Chen J.-P., Su C.-H. Surface modification of electrospun PLLA nanofibers by plasma treatment and cationized gelatin immobilization for cartilage tissue engineering. Acta Biomater. 2011;7(1):234-243.

    Not in our library10.1016/j.actbio.2010.08.015

  105. 105.

    Merkle V.M., Zeng L., Slepian M.J., Wu X. Core-shell nanofibers: integrating the bioactivity of gelatin and the mechanical property of polyvinyl alcohol. Biopolymers. 2014;101(4):336-346.

    Not in our library10.1002/bip.22367

  106. 106.

    Wang D., Wang X., Li X., Jiang L., Chang Z., Li Q. Biologically responsive, long-term release nanocoating on an electrospun scaffold for vascular endothelialization and anticoagulation. Mater. Sci. Eng. C. 2020;107.

    Not in our library10.1016/j.msec.2019.110212

  107. 107.

    Koens M.J.W., Krasznai A.G., Hanssen A.E.J., Hendriks T., Praster R., Daamen W.F., van der Vliet J.A., van Kuppevelt T.H. Vascular replacement using a layered elastin-collagen vascular graft in a porcine model: one week patency versus one month occlusion. Organogenesis. 2015;11(3):105-121.

    Not in our library10.1080/15476278.2015.1038448

  108. 108.

    Grus T., Lambert L., Mlcek M., Chlup H., Honsova E., Spacek M., Burgetova A., Lindner J. In vivo evaluation of short-term performance of new three-layer collagen-based vascular graft designed for low-flow peripheral vascular reconstructions. BioMed Res. Int. 2018.

    Not in our library10.1155/2018/3519596

  109. 109.

    Wang Z., Liu L., Mithieux S.M., Weiss A.S. Fabricating organized elastin in vascular grafts. Trends Biotechnol. 2020.

    Not in our library10.1016/j.tibtech.2020.09.003

  110. 110.

    Gupta P., Lorentz K.L., Haskett D.G., Cunnane E.M., Ramaswamy A.K., Weinbaum J.S., Vorp D.A., Mandal B.B. Bioresorbable silk grafts for small diameter vascular tissue engineering applications: in vitro and in vivo functional analysis. Acta Biomater. 2020;105:146-158.

    Not in our library10.1016/j.actbio.2020.01.020

  111. 111.

    Zhao L., Li X., Yang L., Sun L., Mu S., Zong H., Li Q., Wang F., Song S., Yang C., Zhao C., Chen H., Zhang R., Wang S., Dong Y., Zhang Q. Evaluation of remodeling and regeneration of electrospun PCL/fibrin vascular grafts in vivo. Mater. Sci. Eng. C. 2021;118.

    Not in our library10.1016/j.msec.2020.111441

  112. 112.

    Yu J., Wang A., Tang Z., Henry J., Li-Ping Lee B., Zhu Y., Yuan F., Huang F., Li S. The effect of stromal cell-derived factor-1α/heparin coating of biodegradable vascular grafts on the recruitment of both endothelial and smooth muscle progenitor cells for accelerated regeneration. Biomaterials. 2012;33(32):8062-8074.

    Not in our library10.1016/j.biomaterials.2012.07.042

  113. 113.

    Hersel U., Dahmen C., Kessler H. RGD modified polymers: biomaterials for stimulated cell adhesion and beyond. Biomaterials. 2003;24(24):4385-4415.

    Not in our library10.1016/s0142-9612(03)00343-0

  114. 114.

    Aoki J., Serruys P.W., van Beusekom H., Ong A.T.L., McFadden E.P., Sianos G., van der Giessen W.J., Regar E., de Feyter P.J., Davis H.R., Rowland S., Kutryk M.J.B. Endothelial progenitor cell capture by stents coated with antibody against CD34: the HEALING-FIM (healthy endothelial accelerated lining inhibits neointimal growth-first in man) registry. J. Am. Coll. Cardiol. 2005;45(10):1574-1579.

    Not in our library10.1016/j.jacc.2005.01.048

  115. 115.

    Co M., Tay E., Lee C.H., Poh K.K., Low A., Lim J., Lim I.H., Lim Y.T., Tan H.C. Use of endothelial progenitor cell capture stent (Genous Bio-Engineered R Stent) during primary percutaneous coronary intervention in acute myocardial infarction: intermediate- to long-term clinical follow-up. Am. Heart J. 2008;155(1):128-132.

    Not in our library10.1016/j.ahj.2007.08.031

  116. 116.

    Kaplan D., Husel W., Lewandowska K. CD34 expression on platelets. Platelets. 2003;14(2):83-87.

    Not in our library10.1080/0953710031000080577

  117. 117.

    Yeh E.T.H., Zhang S., Wu H.D., Körbling M., Willerson J.T., Estrov Z. Transdifferentiation of human peripheral blood cd34+-enriched cell population into cardiomyocytes, endothelial cells, and smooth muscle cells in vivo. Circulation. 2003;108(17):2070-2073.

    Not in our library10.1161/01.cir.0000099501.52718.70

  118. 118.

    Sethi R., Lee C.-H. Endothelial progenitor cell capture stent: safety and effectiveness. J. Intervent. Cardiol. 2012;25(5):493-500.

    Not in our library10.1111/j.1540-8183.2012.00740.x

  119. 119.

    Rotmans J.I., Heyligers J.M.M., Verhagen H.J.M., Velema E., Nagtegaal M.M., Kleijn DPVd, Groot FGd, Stroes E.S.G., Pasterkamp G. In vivo cell seeding with anti-CD34 antibodies successfully Accelerates endothelialization but stimulates intimal hyperplasia in porcine arteriovenous expanded polytetrafluoroethylene grafts. Circulation. 2005;112(1):12-18.

    Not in our library10.1161/circulationaha.104.504407

  120. 120.

    Nakazawa G., Granada J.F., Alviar C.L., Tellez A., Kaluza G.L., Guilhermier M.Y., Parker S., Rowland S.M., Kolodgie F.D., Leon M.B., Virmani R. Anti-CD34 antibodies immobilized on the surface of sirolimus-eluting stents enhance stent endothelialization. JACC Cardiovasc. Interv. 2010;3(1):68-75.

    Not in our library10.1016/j.jcin.2009.09.015

  121. 121.

    Haude M., Lee S.W.L., Worthley S.G., Silber S., Verheye S., Erbs S., Rosli M.A., Botelho R., Meredith I., Sim K.H., Stella P.R., Tan H.-C., Whitbourn R., Thambar S., Abizaid A., Koh T.H., Den Heijer P., Parise H., Cristea E., Maehara A., Mehran R. The REMEDEE trial: a randomized comparison of a combination sirolimus-eluting endothelial progenitor cell capture stent with a paclitaxel-eluting stent. JACC Cardiovasc. Interv. 2013;6(4):334-343.

    Not in our library10.1016/j.jcin.2012.10.018

  122. 122.

    Kawahara D., Matsuda T. Hydrodynamic shear-stress-dependent retention of endothelial and endothelial progenitor cells adhered to vascular endothelial growth factor-fixed surfaces. J. Biomed. Mater. Res. B Appl. Biomater. 2012;100B(5):1218-1228.

    Not in our library10.1002/jbm.b.32686

  123. 123.

    Capture of flowing endothelial cells using surface-immobilized anti-kinase insert Domain receptor antibody (2008). Tissue Eng. C Methods 14 (2):97-105. doi:10.1089/ten.tec.2007.0300.

    Not in our library10.1089/ten.tec.2007.0300

  124. 124.

    Liddington R.C., Ginsberg M.H. Integrin activation takes shape. J. Cell Biol. 2002;158(5):833-839.

    Not in our library10.1083/jcb.200206011

  125. 125.

    Lin H.-B., Sun W., Mosher D.F., García-Echeverría C., Schaufelberger K., Lelkes P.I., Cooper S.L. Synthesis, surface, and cell-adhesion properties of polyurethanes containing covalently grafted RGD-peptides. J. Biomed. Mater. Res. 1994;28(3):329-342.

    Not in our library10.1002/jbm.820280307

  126. 126.

    Wang Z., Wang H., Zheng W., Zhang J., Zhao Q., Wang S., Yang Z., Kong D. Highly stable surface modifications of poly(3-caprolactone) (PCL) films by molecular self-assembly to promote cells adhesion and proliferation. Chem Commun. 2011;47(31):8901-8903.

    Not in our library10.1039/c1cc11564b

  127. 127.

    Park J., Brust T.F., Lee H.J., Lee S.C., Watts V.J., Yeo Y. Polydopamine-based simple and versatile surface modification of polymeric nano drug carriers. ACS Nano. 2014;8(4):3347-3356.

    Not in our library10.1021/nn405809c

  128. 128.

    Yang K., Lee J.S., Kim J., Lee Y.B., Shin H., Um S.H., Kim J.B., Park K.I., Lee H., Cho S.-W. Polydopamine-mediated surface modification of scaffold materials for human neural stem cell engineering. Biomaterials. 2012;33(29):6952-6964.

    Not in our library10.1016/j.biomaterials.2012.06.067

  129. 129.

    Sun Y., Deng Y., Ye Z., Liang S., Tang Z., Wei S. Peptide decorated nano-hydroxyapatite with enhanced bioactivity and osteogenic differentiation via polydopamine coating. Colloids Surf. B Biointerfaces. 2013;111:107-116.

    Not in our library10.1016/j.colsurfb.2013.05.037

  130. 130.

    Kanie K., Narita Y., Zhao Y., Kuwabara F., Satake M., Honda S., Kaneko H., Yoshioka T., Okochi M., Honda H., Kato R. Collagen type IV-specific tripeptides for selective adhesion of endothelial and smooth muscle cells. Biotechnol. Bioeng. 2012;109(7):1808-1816.

    Not in our library10.1002/bit.24459

  131. 131.

    Khan M., Yang J., Shi C., Lv J., Feng Y., Zhang W. Surface tailoring for selective endothelialization and platelet inhibition via a combination of SI-ATRP and click chemistry using Cys–Ala–Gly-peptide. Acta Biomater. 2015;20:69-81.

    Not in our library10.1016/j.actbio.2015.03.032

  132. 132.

    Seeto W.J., Tian Y., Lipke E.A. Peptide-grafted poly(ethylene glycol) hydrogels support dynamic adhesion of endothelial progenitor cells. Acta Biomater. 2013;9(9):8279-8289.

    Not in our library10.1016/j.actbio.2013.05.023

  133. 133.

    Lin Q.-K., Hou Y., Ren K.-F., Ji J. Selective endothelial cells adhesion to Arg-Glu-Asp-Val peptide functionalized polysaccharide multilayer. Thin Solid Films. 2012;520(15):4971-4978.

    Not in our library10.1016/j.tsf.2012.03.041

  134. 134.

    Massia S.P., Hubbell J.A. Human endothelial cell interactions with surface-coupled adhesion peptides on a nonadhesive glass substrate and two polymeric biomaterials. J. Biomed. Mater. Res. 1991;25(2):223-242.

    Not in our library10.1002/jbm.820250209

  135. 135.

    Wang P.-Y., Wu T.-H., Tsai W.-B., Kuo W.-H., Wang M.-J. Grooved PLGA films incorporated with RGD/YIGSR peptides for potential application on skeletal muscle tissue engineering. Colloids Surf. B Biointerfaces. 2013;110:88-95.

    Not in our library10.1016/j.colsurfb.2013.04.016

  136. 136.

    Wang W., Guo L., Yu Y., Chen Z., Zhou R., Yuan Z. Peptide REDV-modified polysaccharide hydrogel with endothelial cell selectivity for the promotion of angiogenesis. J. Biomed. Mater. Res. 2015;103(5):1703-1712.

    Not in our library10.1002/jbm.a.35306

  137. 137.

    Wei Y., Ji Y., Xiao L.-L., Lin Q-k, Xu J-p, Ren K-f, Ji J. Surface engineering of cardiovascular stent with endothelial cell selectivity for in vivo re-endothelialisation. Biomaterials. 2013;34(11):2588-2599.

    Not in our library10.1016/j.biomaterials.2012.12.036

  138. 138.

    Plouffe B.D., Njoka D.N., Harris J., Liao J., Horick N.K., Radisic M., Murthy S.K. Peptide-mediated selective adhesion of smooth muscle and endothelial cells in microfluidic shear flow. Langmuir. 2007;23(9):5050-5055.

    Not in our library10.1021/la0700220

  139. 139.

    Ceylan H., Tekinay A.B., Guler M.O. Selective adhesion and growth of vascular endothelial cells on bioactive peptide nanofiber functionalized stainless steel surface. Biomaterials. 2011;32(34):8797-8805.

    Not in our library10.1016/j.biomaterials.2011.08.018

  140. 140.

    Ohuchi S. Cell-SELEX technology. Biores Open Access. 2012;1(6):265-272.

    Not in our library10.1089/biores.2012.0253

  141. 141.

    Hoffmann J., Paul A., Harwardt M., Groll J., Reeswinkel T., Klee D., Moeller M., Fischer H., Walker T., Greiner T., Ziemer G., Wendel H.P. Immobilized DNA aptamers used as potent attractors for porcine endothelial precursor cells. J. Biomed. Mater. Res. 2008;84A(3):614-621.

    Not in our library10.1002/jbm.a.31309

  142. 142.
    Potential capacity of aptamers to trigger immune activation in human blood. · 2013
    Not checked
  143. 143.

    Dvir T., Timko B.P., Kohane D.S., Langer R. Nanotechnological strategies for engineering complex tissues. Nat. Nanotechnol. 2011;6(1):13-22.

    Not in our library10.1038/nnano.2010.246

  144. 144.

    Moffa M., Sciancalepore A.G., Passione L.G., Pisignano D. Combined nano- and micro-scale topographic cues for engineered vascular constructs by electrospinning and imprinted micro-patterns. Small. 2014;10(12):2439-2450.

    Not in our library10.1002/smll.201303179

  145. 145.

    Miller D.C., Webster T.J., Haberstroh K.M. Technological advances in nanoscale biomaterials: the future of synthetic vascular graft design. Expet Rev. Med. Dev. 2004;1(2):259-268.

    Not in our library10.1586/17434440.1.2.259

  146. 146.

    Chong D.S., Lindsey B., Dalby M.J., Gadegaard N., Seifalian A.M., Hamilton G. Luminal surface engineering, 'micro and nanopatterning': potential for self endothelialising vascular grafts? Eur. J. Vasc. Endovasc. Surg. 2014;47(5):566-576.

    Not in our library10.1016/j.ejvs.2014.02.007

  147. 147.

    Xing Q., Qian Z., Tahtinen M., Yap A.H., Yates K., Zhao F. Aligned nanofibrous cell-derived extracellular matrix for Anisotropic vascular graft construction. Adv Healthc Mater. 2017;6(10).

    Not in our library10.1002/adhm.201601333

  148. 148.

    Wu T., Zhang J., Wang Y., Li D., Sun B., El-Hamshary H., Yin M., Mo X. Fabrication and preliminary study of a biomimetic tri-layer tubular graft based on fibers and fiber yarns for vascular tissue engineering. Mater. Sci. Eng. C. 2018;82:121-129.

    Not in our library10.1016/j.msec.2017.08.072

  149. 149.

    Wong C.S., Liu X., Xu Z., Lin T., Wang X. Elastin and collagen enhances electrospun aligned polyurethane as scaffolds for vascular graft. J. Mater. Sci. Mater. Med. 2013;24(8):1865-1874.

    Not in our library10.1007/s10856-013-4937-y

  150. 150.

    Liu R., Qin Y., Wang H., Zhao Y., Hu Z., Wang S. The in vivo blood compatibility of bio-inspired small diameter vascular graft: effect of submicron longitudinally aligned topography. BMC Cardiovasc. Disord. 2013;13:79.

    Not in our library10.1186/1471-2261-13-79

  151. 151.

    Biela S.A., Su Y., Spatz J.P., Kemkemer R. Different sensitivity of human endothelial cells, smooth muscle cells and fibroblasts to topography in the nano–micro range. Acta Biomater. 2009;5(7):2460-2466.

    Not in our library10.1016/j.actbio.2009.04.003

  152. 152.

    Bettinger C.J., Orrick B., Misra A., Langer R., Borenstein J.T. Microfabrication of poly (glycerol–sebacate) for contact guidance applications. Biomaterials. 2006;27(12):2558-2565.

    Not in our library10.1016/j.biomaterials.2005.11.029

  153. 153.

    Cunningham K.S., Gotlieb A.I. The role of shear stress in the pathogenesis of atherosclerosis. Lab. Invest. 2005;85(1):9-23.

    Not in our library10.1038/labinvest.3700215

  154. 154.

    Wang B., Cai Q., Zhang S., Yang X., Deng X. The effect of poly (L-lactic acid) nanofiber orientation on osteogenic responses of human osteoblast-like MG63 cells. Journal of the Mechanical Behavior of Biomedical Materials. 2011;4(4):600-609.

    Not in our library10.1016/j.jmbbm.2011.01.008

  155. 155.

    Liliensiek S.J., Wood J.A., Yong J., Auerbach R., Nealey P.F., Murphy C.J. Modulation of human vascular endothelial cell behaviors by nanotopographic cues. Biomaterials. 2010;31(20):5418-5426.

    Not in our library10.1016/j.biomaterials.2010.03.045

  156. 156.

    Morgan J.T., Wood J.A., Shah N.M., Hughbanks M.L., Russell P., Barakat A.I., Murphy C.J. Integration of basal topographic cues and apical shear stress in vascular endothelial cells. Biomaterials. 2012;33(16):4126-4135.

    Not in our library10.1016/j.biomaterials.2012.02.047

  157. 157.

    Ding Y., Yang Z., Bi C.W.C., Yang M., Xu S.L., Lu X., Huang N., Huang P., Leng Y. Directing vascular cell selectivity and hemocompatibility on patterned platforms Featuring variable topographic Geometry and size. ACS Appl. Mater. Interfaces. 2014;6(15):12062-12070.

    Not in our library10.1021/am502692k

  158. 158.

    Seunarine K., Meredith D.O., Riehle M.O., Wilkinson C.D.W., Gadegaard N. Biodegradable polymer tubes with lithographically controlled 3D micro- and nanotopography. Microelectron. Eng. 2008;85(5):1350-1354.

    Not in our library10.1016/j.mee.2008.02.002

  159. 159.

    Zhou K., Li Y., Zhang L., Jin L., Yuan F., Tan J., Yuan G., Pei J. Nano-micrometer surface roughness gradients reveal topographical influences on differentiating responses of vascular cells on biodegradable magnesium. Bioactive Materials. 2021;6(1):262-272.

    Not in our library10.1016/j.bioactmat.2020.08.004

  160. 160.

    Wang Z., Liu C., Xiao Y., Gu X., Xu Y., Dong N., Zhang S., Qin Q., Wang J. Remodeling of a cell-free vascular graft with Nanolamellar intima into a Neovessel. ACS Nano. 2019;13(9):10576-10586.

    Not in our library10.1021/acsnano.9b04704

  161. 161.

    Zorlutuna P., Vadgama P., Hasirci V. Both sides nanopatterned tubular collagen scaffolds as tissue-engineered vascular grafts. J Tissue Eng Regen Med. 2010;4(8):628-637.

    Not in our library10.1002/term.278

  162. 162.

    Le Saux G., Magenau A., Gunaratnam K., Kilian K.A., Böcking T., Gooding J.J., Gaus K. Spacing of integrin ligands influences signal transduction in endothelial cells. Biophys. J. 2011;101(4):764-773.

    Not in our library10.1016/j.bpj.2011.06.064

  163. 163.

    Wang X., Yan C., Ye K., He Y., Li Z., Ding J. Effect of RGD nanospacing on differentiation of stem cells. Biomaterials. 2013;34(12):2865-2874.

    Not in our library10.1016/j.biomaterials.2013.01.021

  164. 164.

    Le Saux G., Magenau A., Böcking T., Gaus K., Gooding J.J. The relative importance of topography and RGD ligand density for endothelial cell adhesion. PloS One. 2011;6(7).

    Not in our library10.1371/journal.pone.0021869

  165. 165.

    Karimi F., McKenzie T.G., O'Connor A.J., Qiao G.G., Heath D.E. Nano-scale clustering of integrin-binding ligands regulates endothelial cell adhesion, migration, and endothelialization rate: novel materials for small diameter vascular graft applications. J. Mater. Chem. B. 2017;5(30):5942-5953.

    Not in our library10.1039/c7tb01298e

  166. 166.

    Eichmann A., Simons M. VEGF signaling inside vascular endothelial cells and beyond. Curr. Opin. Cell Biol. 2012;24(2):188-193.

    Not in our library10.1016/j.ceb.2012.02.002

  167. 167.

    Ferrara N., Gerber H.-P., LeCouter J. The biology of VEGF and its receptors. Nat. Med. 2003;9(6):669-676.

    Not in our library10.1038/nm0603-669

  168. 168.

    Shin Y.M., Lee Y.B., Kim S.J., Kang J.K., Park J.-C., Jang W., Shin H. Mussel-Inspired immobilization of vascular endothelial growth factor (VEGF) for enhanced endothelialization of vascular grafts. Biomacromolecules. 2012;13(7):2020-2028.

    Not in our library10.1021/bm300194b

  169. 169.

    Zhang J., Silva T., Yarovinsky T., Manes T.D., Tavakoli S., Nie L., Tellides G., Pober J.S., Bender J.R., Sadeghi M.M. VEGF blockade inhibits lymphocyte recruitment and Ameliorates immune-mediated vascular remodeling. Circ. Res. 2010;107(3):408-417.

    Not in our library10.1161/circresaha.109.210963

  170. 170.

    Tan Q., Tang H., Hu J., Hu Y., Zhou X., Tao Y., Wu Z. Controlled release of chitosan/heparin nanoparticle-delivered VEGF enhances regeneration of decellularized tissue-engineered scaffolds. Int. J. Nanomed. 2011;6:929-942.

    Not in our library10.2147/ijn.s18753

  171. 171.

    Hu Y.-T., Pan X.-D., Zheng J., Ma W.-G., Sun L.-Z. In vitro and in vivo evaluation of a small-caliber coaxial electrospun vascular graft loaded with heparin and VEGF. Int. J. Surg. 2017;44:244-249.

    Not in our library10.1016/j.ijsu.2017.06.077

  172. 172.

    Yang B., Cao G., Cai K., Wang G., Li P., Zheng L., Cai H., Zhu Y., Li X., Wu Y. VEGF-modified PVA/silicone nanofibers enhance islet function transplanted in subcutaneous site followed by Device-less procedure. Int. J. Nanomed. 2020;15:587-599.

    Not in our library10.2147/ijn.s232224

  173. 173.

    Zhou F., Jia X., Yang Y., Yang Q., Gao C., Hu S., Zhao Y., Fan Y., Yuan X. Nanofiber-mediated microRNA-126 delivery to vascular endothelial cells for blood vessel regeneration. Acta Biomater. 2016;43:303-313.

    Not in our library10.1016/j.actbio.2016.07.048

  174. 174.

    Miyazu K., Kawahara D., Ohtake H., Watanabe G., Matsuda T. Luminal surface design of electrospun small-diameter graft aiming at in situ capture of endothelial progenitor cell. J. Biomed. Mater. Res. B Appl. Biomater. 2010;94(1):53-63.

    Not in our library10.1002/jbm.b.31623

  175. 175.

    Suzuki Y., Yamamoto K., Ando J., Matsumoto K., Matsuda T. Arterial shear stress augments the differentiation of endothelial progenitor cells adhered to VEGF-bound surfaces. Biochem. Biophys. Res. Commun. 2012;423(1):91-97.

    Not in our library10.1016/j.bbrc.2012.05.088

  176. 176.

    Cho Y., Lee J.B., Hong J. Tunable growth factor release from nano-assembled starch multilayers. Chem. Eng. J. 2013;221:32-36.

    Not in our library10.1016/j.cej.2013.01.087

  177. 177.

    Park J.H., Hong J. Continuous release of bFGF from multilayer nanofilm to maintain undifferentiated human iPS cell cultures. Integr Biol (Camb). 2014;6(12):1196-1200.

    Not in our library10.1039/c4ib00210e

  178. 178.

    Rajangam K., Arnold M.S., Rocco M.A., Stupp S.I. Peptide amphiphile nanostructure–heparin interactions and their relationship to bioactivity. Biomaterials. 2008;29(23):3298-3305.

    Not in our library10.1016/j.biomaterials.2008.04.008

  179. 179.

    Zhang H., Jia X., Han F., Zhao J., Zhao Y., Fan Y., Yuan X. Dual-delivery of VEGF and PDGF by double-layered electrospun membranes for blood vessel regeneration. Biomaterials. 2013;34(9):2202-2212.

    Not in our library10.1016/j.biomaterials.2012.12.005

  180. 180.

    Han F., Jia X., Dai D., Yang X., Zhao J., Zhao Y., Fan Y., Yuan X. Performance of a multilayered small-diameter vascular scaffold dual-loaded with VEGF and PDGF. Biomaterials. 2013;34(30):7302-7313.

    Not in our library10.1016/j.biomaterials.2013.06.006

  181. 181.

    Khanna O., Huang J.-J., Moya M.L., Wu C.-W., Cheng M.-H., Opara E.C., Brey E.M. FGF-1 delivery from multilayer alginate microbeads stimulates a rapid and persistent increase in vascular density. Microvasc. Res. 2013;90:23-29.

    Not in our library10.1016/j.mvr.2013.08.006

  182. 182.

    Selcan Gungor-Ozkerim P., Balkan T., Kose G.T., Sezai Sarac A., Kok F.N. Incorporation of growth factor loaded microspheres into polymeric electrospun nanofibers for tissue engineering applications. J. Biomed. Mater. Res. 2014;102(6):1897-1908.

    Not in our library10.1002/jbm.a.34857

  183. 183.

    Poldervaart M.T., Gremmels H., van Deventer K., Fledderus J.O., Öner F.C., Verhaar M.C., Dhert W.J.A., Alblas J. Prolonged presence of VEGF promotes vascularization in 3D bioprinted scaffolds with defined architecture. J. Contr. Release. 2014;184:58-66.

    Not in our library10.1016/j.jconrel.2014.04.007

  184. 184.

    Ev Rooij. The Art of MicroRNA research. Circ. Res. 2011;108(2):219-234.

    Not in our library10.1161/circresaha.110.227496

  185. 185.

    Feinberg M.W., Moore K.J. MicroRNA regulation of atherosclerosis. Circ. Res. 2016;118(4):703-720.

    Not in our library10.1161/circresaha.115.306300

  186. 186.

    Wang S., Aurora A.B., Johnson B.A., Qi X., McAnally J., Hill J.A., Richardson J.A., Bassel-Duby R., Olson E.N. The endothelial-specific MicroRNA miR-126 Governs vascular integrity and angiogenesis. Dev. Cell. 2008;15(2):261-271.

    Not in our library10.1016/j.devcel.2008.07.002

  187. 187.

    Fish J.E., Santoro M.M., Morton S.U., Yu S., Yeh R.-F., Wythe J.D., Ivey K.N., Bruneau B.G., Stainier D.Y.R., Srivastava D. miR-126 regulates angiogenic signaling and vascular integrity. Dev. Cell. 2008;15(2):272-284.

    Not in our library10.1016/j.devcel.2008.07.008

  188. 188.

    Cui C., Wen M., Zhou F., Zhao Y., Yuan X. Target regulation of both VECs and VSMCs by dual-loading miRNA-126 and miRNA-145 in the bilayered electrospun membrane for small-diameter vascular regeneration. J. Biomed. Mater. Res. 2019;107(2):371-382.

    Not in our library10.1002/jbm.a.36548

  189. 189.
    MicroRNA-22 Inhibits the Apoptosis of Vascular Smooth Muscle Cell by Targeting p38MAPKα in Vascular Remodeling of Aortic Dissection · 2020
    Not checked
  190. 190.

    Lu J.-M., Zhang Z.-Z., Ma X., Fang S.-F., Qin X.-H. Repression of microRNA-21 inhibits retinal vascular endothelial cell growth and angiogenesis via PTEN dependent-PI3K/Akt/VEGF signaling pathway in diabetic retinopathy. Exp. Eye Res. 2020;190.

    Not in our library10.1016/j.exer.2019.107886

  191. 191.

    de Mel A., Murad F., Seifalian A.M. Nitric oxide: a Guardian for vascular grafts? Chem. Rev. 2011;111(9):5742-5767.

    Not in our library10.1021/cr200008n

  192. 192.

    Andukuri A., Sohn Y.D., Anakwenze C.P., Lim D.J., Brott B.C., Yoon Y.S., Jun H.W. Enhanced human endothelial progenitor cell adhesion and differentiation by a bioinspired multifunctional nanomatrix. Tissue Eng. C Methods. 2013;19(5):375-385.

    Not in our library10.1089/ten.tec.2012.0312

  193. 193.

    Lou D., Luo Y., Pang Q., Tan W.-Q., Ma L. Gene-activated dermal equivalents to accelerate healing of diabetic chronic wounds by regulating inflammation and promoting angiogenesis. Bioactive Materials. 2020;5(3):667-679.

    Not in our library10.1016/j.bioactmat.2020.04.018

  194. 194.

    Lajunen T., Hisazumi K., Kanazawa T., Okada H., Seta Y., Yliperttula M., Urtti A., Takashima Y. Topical drug delivery to retinal pigment epithelium with microfluidizer produced small liposomes. Eur. J. Pharmaceut. Sci. 2014;62:23-32.

    Not in our library10.1016/j.ejps.2014.04.018

  195. 195.

    Negishi Y., Tsunoda Y., Hamano N., Omata D., Endo-Takahashi Y., Suzuki R., Maruyama K., Nomizu M., Aramaki Y. Ultrasound-mediated gene delivery systems by AG73-modified bubble liposomes. Peptide Science. 2013;100(4):402-407.

    Not in our library10.1002/bip.22246

  196. 196.

    Carr L.R., Jiang S. Mediating high levels of gene transfer without cytotoxicity via hydrolytic cationic ester polymers. Biomaterials. 2010;31(14):4186-4193.

    Not in our library10.1016/j.biomaterials.2010.01.110

  197. 197.

    Huang Z., Teng W., Liu L., Wang L., Wang Q., Dong Y. Efficient cytosolic delivery mediated by polymersomes facilely prepared from a degradable, amphiphilic, and amphoteric copolymer. Nanotechnology. 2013;24(26):265104.

    Not in our library10.1088/0957-4484/24/26/265104

  198. 198.

    Teng W., Huang Z., Chen Y., Wang L., Wang Q., Huang H. pVEGF-loaded lipopolysaccharide-amine nanopolymersomes for therapeutic angiogenesis. Nanotechnology. 2014;25(6).

    Not in our library10.1088/0957-4484/25/6/065702

  199. 199.

    Zhang J., Wang Z., Lin W., Chen S. Gene transfection in complex media using PCBMAEE-PCBMA copolymer with both hydrolytic and zwitterionic blocks. Biomaterials. 2014;35(27):7909-7918.

    Not in our library10.1016/j.biomaterials.2014.05.066

  200. 200.

    Calarco A., Bosetti M., Margarucci S., Fusaro L., Nicolì E., Petillo O., Cannas M., Galderisi U., Peluso G. The genotoxicity of PEI-based nanoparticles is reduced by acetylation of polyethylenimine amines in human primary cells. Toxicol. Lett. 2013;218(1):10-17.

    Not in our library10.1016/j.toxlet.2012.12.019

  201. 201.

    Zheng M., Zhong Z., Zhou L., Meng F., Peng R., Zhong Z. Poly(ethylene oxide) grafted with short polyethylenimine Gives DNA polyplexes with superior colloidal stability, low cytotoxicity, and potent in vitro gene transfection under serum conditions. Biomacromolecules. 2012;13(3):881-888.

    Not in our library10.1021/bm2017965

  202. 202.

    Li Q., Shi C., Zhang W., Behl M., Lendlein A., Feng Y. Nanoparticles complexed with gene vectors to promote proliferation of human vascular endothelial cells. Advanced Healthcare Materials. 2015;4(8):1225-1235.

    Not in our library10.1002/adhm.201400817

  203. 203.

    Chen F., Wan H., Xia T., Guo X., Wang H., Liu Y., Li X. Promoted regeneration of mature blood vessels by electrospun fibers with loaded multiple pDNA-calcium phosphate nanoparticles. Eur. J. Pharm. Biopharm. 2013;85(3):699-710.

    Not in our library10.1016/j.ejpb.2013.07.009

  204. 204.

    Qu W., Qin S.-Y., Ren S., Jiang X.-J., Zhuo R.-X., Zhang X.-Z. Peptide-based vector of VEGF plasmid for efficient gene delivery in vitro and vessel formation in vivo. Bioconjugate Chem. 2013;24(6):960-967.

    Not in our library10.1021/bc300677n

  205. 205.

    He S., Xia T., Wang H., Wei L., Luo X., Li X. Multiple release of polyplexes of plasmids VEGF and bFGF from electrospun fibrous scaffolds towards regeneration of mature blood vessels. Acta Biomater. 2012;8(7):2659-2669.

    Not in our library10.1016/j.actbio.2012.03.044

  206. 206.

    Luu Y.K., Kim K., Hsiao B.S., Chu B., Hadjiargyrou M. Development of a nanostructured DNA delivery scaffold via electrospinning of PLGA and PLA–PEG block copolymers. J. Contr. Release. 2003;89(2):341-353.

    Not in our library10.1016/s0168-3659(03)00097-x

  207. 207.

    Yu L., Feng Y., Li Q., Hao X., Liu W., Zhou W., Shi C., Ren X., Zhang W. PLGA/SF blend scaffolds modified with plasmid complexes for enhancing proliferation of endothelial cells. React. Funct. Polym. 2015;91–92:19-27.

    Not in our library10.1016/j.reactfunctpolym.2015.04.003

  208. 208.

    Anwer K., Kao G., Rolland A., Driessen W.H.P., Sullivan S.M. Peptide-mediated gene transfer of cationic lipid/plasmid DNA complexes to endothelial cells. J. Drug Target. 2004;12(4):215-221.

    Not in our library10.1080/10611860410001724468

  209. 209.

    Suh W., Han S.O., Yu L., Kim S.W. An angiogenic, endothelial-cell-targeted polymeric gene carrier. Mol. Ther. 2002;6(5):664-672.

    Not in our library

  210. 210.

    Wang H., Feng Y., Yang J., Guo J., Zhang W. Targeting REDV peptide functionalized polycationic gene carrier for enhancing the transfection and migration capability of human endothelial cells. J. Mater. Chem. B. 2015;3(16):3379-3391.

    Not in our library10.1039/c4tb02019g

  211. 211.

    Kibria G., Hatakeyama H., Ohga N., Hida K., Harashima H. Dual-ligand modification of PEGylated liposomes shows better cell selectivity and efficient gene delivery. J. Contr. Release. 2011;153(2):141-148.

    Not in our library10.1016/j.jconrel.2011.03.012

  212. 212.

    Chen J., Dai S., Liu L., Maitz M.F., Liao Y., Cui J., Zhao A., Yang P., Huang N., Wang Y. Photo-functionalized TiO2 nanotubes decorated with multifunctional Ag nanoparticles for enhanced vascular biocompatibility. Bioactive Materials. 2021;6(1):45-54.

    Not in our library10.1016/j.bioactmat.2020.07.009

  213. 213.

    Neffe A.T., von Ruesten-Lange M., Braune S., Luetzow K., Roch T., Richau K., Jung F., Lendlein A. Poly(ethylene glycol) grafting to poly(ether imide) membranes: influence on protein adsorption and thrombocyte adhesion. Macromol. Biosci. 2013;13(12):1720-1729.

    Not in our library10.1002/mabi.201300309

  214. 214.

    Cai X., Yuan J., Chen S., Li P., Li L., Shen J. Hemocompatibility improvement of poly(ethylene terephthalate) via self-polymerization of dopamine and covalent graft of zwitterions. Mater. Sci. Eng. C. 2014;36:42-48.

    Not in our library10.1016/j.msec.2013.11.038

  215. 215.

    Feng W., Brash J.L., Zhu S. Non-biofouling materials prepared by atom transfer radical polymerization grafting of 2-methacryloloxyethyl phosphorylcholine: separate effects of graft density and chain length on protein repulsion. Biomaterials. 2006;27(6):847-855.

    Not in our library10.1016/j.biomaterials.2005.07.006

  216. 216.

    Takahashi N., Iwasa F., Inoue Y., Morisaki H., Ishihara K., Baba K. Evaluation of the durability and antiadhesive action of 2-methacryloyloxyethyl phosphorylcholine grafting on an acrylic resin denture base material. J. Prosthet. Dent. 2014;112(2):194-203.

    Not in our library10.1016/j.prosdent.2013.08.020

  217. 217.

    Su Y., Li C., Zhao W., Shi Q., Wang H., Jiang Z., Zhu S. Modification of polyethersulfone ultrafiltration membranes with phosphorylcholine copolymer can remarkably improve the antifouling and permeation properties. J. Membr. Sci. 2008;322(1):171-177.

    Not in our library10.1016/j.memsci.2008.05.047

  218. 218.

    Xiaofen H., Gongyan L., Jian J., Dezeng F., Xinhao Y. Lipid-like Diblock copolymer as an Additive for improving the blood compatibility of poly(lactide-co-glycolide). J. Bioact. Compat Polym. 2010;25(6):654-668.

    Not in our library10.1177/0883911510384836

  219. 219.

    Feng Y., Tian H., Tan M., Zhang P., Chen Q., Liu J. Surface modification of polycarbonate urethane by covalent linkage of heparin with a PEG spacer. Trans. Tianjin Univ. 2013;19(1):58-65.

    Not in our library10.1007/s12209-013-1894-y

  220. 220.

    Liu P., Chen Q., Li L., Lin S., Shen J. Anti-biofouling ability and cytocompatibility of the zwitterionic brushes-modified cellulose membrane. J. Mater. Chem. B. 2014;2(41):7222-7231.

    Not in our library10.1039/c4tb01151a

  221. 221.

    Liu T., Zeng Z., Liu Y., Wang J., Maitz M.F., Wang Y., Liu S., Chen J., Huang N. Surface modification with dopamine and heparin/poly-l-lysine nanoparticles provides a favorable release behavior for the healing of vascular stent Lesions. ACS Appl. Mater. Interfaces. 2014;6(11):8729-8743.

    Not in our library10.1021/am5015309

  222. 222.

    Tan M., Feng Y., Wang H., Zhang L., Khan M., Guo J., Chen Q., Liu J. Immobilized bioactive agents onto polyurethane surface with heparin and phosphorylcholine group. Macromol. Res. 2013;21(5):541-549.

    Not in our library10.1007/s13233-013-1028-3

  223. 223.

    Cheng Q., Komvopoulos K., Li S. Plasma-assisted heparin conjugation on electrospun poly(L-lactide) fibrous scaffolds. J. Biomed. Mater. Res. 2014;102(5):1408-1414.

    Not in our library10.1002/jbm.a.34802

  224. 224.

    Wang H., Feng Y., Zhao H., Xiao R., Lu J., Zhang L., Guo J. Electrospun hemocompatible PU/gelatin-heparin nanofibrous bilayer scaffolds as potential artificial blood vessels. Macromol. Res. 2012;20(4):347-350.

    Not in our library10.1007/s13233-012-0012-7

  225. 225.

    Liu T., Liu Y., Chen Y., Liu S., Maitz M.F., Wang X., Zhang K., Wang J., Wang Y., Chen J., Huang N. Immobilization of heparin/poly-l-lysine nanoparticles on dopamine-coated surface to create a heparin density gradient for selective direction of platelet and vascular cells behavior. Acta Biomater. 2014;10(5):1940-1954.

    Not in our library10.1016/j.actbio.2013.12.013

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    Elahi M.F., Guan G., Wang L., King M.W. Improved hemocompatibility of silk fibroin fabric using layer-by-layer polyelectrolyte deposition and heparin immobilization. J. Appl. Polym. Sci. 2014;131(18).

    Not in our library10.1002/app.40772

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    Easton C.D., Bullock A.J., Gigliobianco G., McArthur S.L., MacNeil S. Application of layer-by-layer coatings to tissue scaffolds – development of an angiogenic biomaterial. J. Mater. Chem. B. 2014;2(34):5558-5568.

    Not in our library10.1039/c4tb00448e

  228. 228.

    Liu W., Wu Z., Wang Y., Tang Z., Du J., Yuan L., Li D., Chen H. Controlling the biointerface of electrospun mats for clot lysis: an engineered tissue plasminogen activator link to a lysine-functionalized surface. J. Mater. Chem. B. 2014;2(27):4272-4279.

    Not in our library10.1039/c4tb00488d

  229. 229.

    Absar S., Choi S., Yang V.C., Kwon Y.M. Heparin-triggered release of camouflaged tissue plasminogen activator for targeted thrombolysis. J. Contr. Release. 2012;157(1):46-54.

    Not in our library10.1016/j.jconrel.2011.09.060

  230. 230.

    Ahmed M., Ghanbari H., Cousins B.G., Hamilton G., Seifalian A.M. Small calibre polyhedral oligomeric silsesquioxane nanocomposite cardiovascular grafts: influence of porosity on the structure, haemocompatibility and mechanical properties. Acta Biomater. 2011;7(11):3857-3867.

    Not in our library10.1016/j.actbio.2011.06.051

  231. 231.

    Ahmed M., Hamilton G., Seifalian A.M. The performance of a small-calibre graft for vascular reconstructions in a senescent sheep model. Biomaterials. 2014;35(33):9033-9040.

    Not in our library10.1016/j.biomaterials.2014.07.008

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    Chong D.S.T., Turner L.A., Gadegaard N., Seifalian A.M., Dalby M.J., Hamilton G. Nanotopography and plasma treatment: redesigning the surface for vascular graft endothelialisation. Eur. J. Vasc. Endovasc. Surg. 2015;49(3):335-343.

    Not in our library10.1016/j.ejvs.2014.12.008

  233. 233.

    Kannan R.Y., Salacinski H.J., Odlyha M., Butler P.E., Seifalian A.M. The degradative resistance of polyhedral oligomeric silsesquioxane nanocore integrated polyurethanes: an in vitro study. Biomaterials. 2006;27(9):1971-1979.

    Not in our library10.1016/j.biomaterials.2005.10.006

  234. 234.

    Kent K.C., Liu B. Intimal hyperplasia—still Here after All these years! Ann. Vasc. Surg. 2004;18(2):135-137.

    Not in our library10.1007/s10016-004-0019-4

  235. 235.

    Zhao Y., Zang G., Yin T., Ma X., Zhou L., Wu L., Daniel R., Wang Y., Qiu J., Wang G. A novel mechanism of inhibiting in-stent restenosis with arsenic trioxide drug-eluting stent: enhancing contractile phenotype of vascular smooth muscle cells via YAP pathway. Bioactive Materials. 2021;6(2):375-385.

    Not in our library10.1016/j.bioactmat.2020.08.018

  236. 236.

    Conte M.S., Bandyk D.F., Clowes A.W., Moneta G.L., Seely L., Lorenz T.J., Namini H., Hamdan A.D., Roddy S.P., Belkin M., Berceli S.A., DeMasi R.J., Samson R.H., Berman S.S. Results of PREVENT III: a multicenter, randomized trial of edifoligide for the prevention of vein graft failure in lower extremity bypass surgery. J. Vasc. Surg. 2006;43(4):742-751.

    Not in our library10.1016/j.jvs.2005.12.058

  237. 237.

    Alexander J.H., Hafley G., Harrington R.A., Peterson E.D., Ferguson T.B., Lorenz T.J., Goyal A., Gibson M., Mack M.J., Gennevois D., Califf R.M., Kouchoukos N.T. Efficacy and safety of edifoligide, an E2F transcription factor decoy, for prevention of vein graft failure following coronary artery bypass graft surgery: prevent IV: a randomized controlled trial. J. Am. Med. Assoc. 2005;294(19):2446-2454.

    Not in our library10.1001/jama.294.19.2446

  238. 238.

    Bakin A.V., Rinehart C., Tomlinson A.K., Arteaga C.L. p38 mitogen-activated protein kinase is required for TGFbeta-mediated fibroblastic transdifferentiation and cell migration. J. Cell Sci. 2002;115(Pt 15):3193-3206.

    Not in our library10.1242/jcs.115.15.3193

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    Hedges J.C., Dechert M.A., Yamboliev I.A., Martin J.L., Hickey E., Weber L.A., Gerthoffer W.T. A role for p38(MAPK)/HSP27 pathway in smooth muscle cell migration. J. Biol. Chem. 1999;274(34):24211-24219.

    Not in our library10.1074/jbc.274.34.24211

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    Rousseau S., Morrice N., Peggie M., Campbell D.G., Gaestel M., Cohen P. Inhibition of SAPK2a/p38 prevents hnRNP A0 phosphorylation by MAPKAP-K2 and its interaction with cytokine mRNAs. EMBO J. 2002;21(23):6505-6514.

    Not in our library10.1093/emboj/cdf639

  241. 241.

    Evans B.C., Hocking K.M., Osgood M.J., Voskresensky I., Dmowska J., Kilchrist K.V., Brophy C.M., Duvall C.L. MK2 inhibitory peptide delivered in nanopolyplexes prevents vascular graft intimal hyperplasia. Sci. Transl. Med. 2015;7(291).

    Not in our library10.1126/scitranslmed.aaa4549

  242. 242.

    Yang Y., Gao P., Wang J., Tu Q., Bai L., Xiong K., Qiu H., Zhao X., Maitz M.F., Wang H., Li X., Zhao Q., Xiao Y., Huang N., Yang Z. Endothelium-Mimicking Multifunctional Coating Modified Cardiovascular Stents via a Stepwise Metal-Catechol-(Amine) Surface Engineering Strategy. 2020.

    Not in our library10.34133/2020/9203906

  243. 243.

    Naghavi N., de Mel A., Alavijeh O.S., Cousins B.G., Seifalian A.M. Nitric oxide donors for cardiovascular implant applications. Small. 2013;9(1):22-35.

    Not in our library10.1002/smll.201200458

  244. 244.

    Zhang F., Zhang Q., Li X., Huang N., Zhao X., Yang Z. Mussel-inspired dopamine-CuII coatings for sustained in situ generation of nitric oxide for prevention of stent thrombosis and restenosis. Biomaterials. 2019;194:117-129.

    Not in our library10.1016/j.biomaterials.2018.12.020

  245. 245.

    de Mel A., Jell G., Stevens M.M., Seifalian A.M. Biofunctionalization of biomaterials for accelerated in situ endothelialization: a review. Biomacromolecules. 2008;9(11):2969-2979.

    Not in our library10.1021/bm800681k

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    Elnaggar M.A., Seo S.H., Gobaa S., Lim K.S., Bae I.-H., Jeong M.H., Han D.K., Joung Y.K. Nitric oxide releasing coronary stent: a new approach using layer-by-layer coating and liposomal encapsulation. Small. 2016;12(43):6012-6023.

    Not in our library10.1002/smll.201600337

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    Tanner F.C., Meier P., Greutert H., Champion C., Nabel E.G., Lüscher T.F. Nitric oxide modulates expression of cell cycle regulatory proteins: a cytostatic strategy for inhibition of human vascular smooth muscle cell proliferation. Circulation. 2000;101(16):1982-1989.

    Not in our library10.1161/01.cir.101.16.1982

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    Elnaggar M.A., Subbiah R., Han D.K., Joung Y.K. Lipid-based carriers for controlled delivery of nitric oxide. Expet Opin. Drug Deliv. 2017;14(12):1341-1353.

    Not in our library10.1080/17425247.2017.1285904

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    Qiu H., Qi P., Liu J., Yang Y., Tan X., Xiao Y., Maitz M.F., Huang N., Yang Z. Biomimetic engineering endothelium-like coating on cardiovascular stent through heparin and nitric oxide-generating compound synergistic modification strategy. Biomaterials. 2019;207:10-22.

    Not in our library10.1016/j.biomaterials.2019.03.033

  250. 250.

    Hrabie J.A., Keefer L.K. Chemistry of the nitric oxide-releasing diazeniumdiolate (“Nitrosohydroxylamine”) functional group and its oxygen-substituted Derivatives. Chem. Rev. 2002;102(4):1135-1154.

    Not in our library10.1021/cr000028t

  251. 251.

    Al-Sa'doni H., Ferro A. S-Nitrosothiols: a class of nitric oxide-donor drugs. Clin. Sci. (Lond.). 2000;98(5):507-520.

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    Al-Sa'doni H.H., Ferro A. S-nitrosothiols as nitric oxide-donors: chemistry, biology and possible future therapeutic applications. Curr. Med. Chem. 2004;11(20):2679-2690.

    Not in our library10.2174/0929867043364397

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    Yang Z., Yang Y., Xiong K., Wang J., Lee H., Huang N. Metal-phenolic surfaces for generating therapeutic nitric oxide gas. Chem. Mater. 2018;30(15):5220-5226.

    Not in our library10.1021/acs.chemmater.8b01876

  254. 254.

    Yang Z., Yang Y., Zhang L., Xiong K., Li X., Zhang F., Wang J., Zhao X., Huang N. Mussel-inspired catalytic selenocystamine-dopamine coatings for long-term generation of therapeutic gas on cardiovascular stents. Biomaterials. 2018;178:1-10.

    Not in our library10.1016/j.biomaterials.2018.06.008

  255. 255.

    Fan Y., Zhang Y., Zhao Q., Xie Y., Luo R., Yang P., Weng Y. Immobilization of nano Cu-MOFs with polydopamine coating for adaptable gasotransmitter generation and copper ion delivery on cardiovascular stents. Biomaterials. 2019;204:36-45.

    Not in our library10.1016/j.biomaterials.2019.03.007

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    Saraiva J., Marotta-Oliveira S.S., Cicillini S.A., Eloy Jde O., Marchetti J.M. Nanocarriers for nitric oxide delivery. Journal of drug delivery. 2011;2011.

    Not in our library10.1155/2011/936438

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    Carpenter A.W., Slomberg D.L., Rao K.S., Schoenfisch M.H. Influence of scaffold size on bactericidal activity of nitric oxide-releasing silica nanoparticles. ACS Nano. 2011;5(9):7235-7244.

    Not in our library10.1021/nn202054f

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    Frost M.C., Meyerhoff M.E. Synthesis, characterization, and controlled nitric oxide release from S-nitrosothiol-derivatized fumed silica polymer filler particles. J. Biomed. Mater. Res. 2005;72(4):409-419.

    Not in our library10.1002/jbm.a.30275

  259. 259.

    Zhang H., Annich G.M., Miskulin J., Stankiewicz K., Osterholzer K., Merz S.I., Bartlett R.H., Meyerhoff M.E. Nitric oxide-releasing fumed silica particles: synthesis, characterization, and biomedical application. J. Am. Chem. Soc. 2003;125(17):5015-5024.

    Not in our library10.1021/ja0291538

  260. 260.

    Huang S.L., Kee P.H., Kim H., Moody M.R., Chrzanowski S.M., Macdonald R.C., McPherson D.D. Nitric oxide-loaded echogenic liposomes for nitric oxide delivery and inhibition of intimal hyperplasia. J. Am. Coll. Cardiol. 2009;54(7):652-659.

    Not in our library10.1016/j.jacc.2009.04.039

  261. 261.

    Dinh B., Dove K., Jappar D., Hrabie J.A., Davies K.M. Effect of hydrophobic structure on the catalysis of nitric oxide release from zwitterionic diazeniumdiolates in surfactant and liposome media. Nitric Oxide. 2005;13(3):204-209.

    Not in our library10.1016/j.niox.2005.07.003

  262. 262.

    Shin J.H., Metzger S.K., Schoenfisch M.H. Synthesis of nitric oxide-releasing silica nanoparticles. J. Am. Chem. Soc. 2007;129(15):4612-4619.

    Not in our library10.1021/ja0674338

  263. 263.

    Shin J.H., Schoenfisch M.H. Inorganic/organic hybrid silica nanoparticles as a nitric oxide delivery scaffold. Chem. Mater. 2008;20(1):239-249.

    Not in our library10.1021/cm702526q

  264. 264.

    Malam Y., Loizidou M., Seifalian A.M. Liposomes and nanoparticles: nanosized vehicles for drug delivery in cancer. Trends Pharmacol. Sci. 2009;30(11):592-599.

    Not in our library10.1016/j.tips.2009.08.004

  265. 265.

    Dinh B.T., Price S.E., Majul A., El-Hajj M., Morozov V., Hrabie J.A., Davies K.M. Diazeniumdiolate reactivity in model membrane systems. Nitric Oxide. 2008;18(2):113-121.

    Not in our library10.1016/j.niox.2007.11.001

  266. 266.

    Tai L.A., Wang Y.C., Yang C.S. Heat-activated sustaining nitric oxide release from zwitterionic diazeniumdiolate loaded in thermo-sensitive liposomes. Nitric Oxide. 2010;23(1):60-64.

    Not in our library10.1016/j.niox.2010.04.003

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    Koehler J.J., Zhao J., Jedlicka S.S., Porterfield D.M., Rickus J.L. Compartmentalized nanocomposite for dynamic nitric oxide release. J. Phys. Chem. B. 2008;112(47):15086-15093.

    Not in our library10.1021/jp803276u

  268. 268.

    Templeton A.C., Wuelfing W.P., Murray R.W. Monolayer-protected cluster molecules. Acc. Chem. Res. 2000;33(1):27-36.

    Not in our library10.1021/ar9602664

  269. 269.

    Jain S., Hirst D.G., O'Sullivan J.M. Gold nanoparticles as novel agents for cancer therapy. Br. J. Radiol. 2012;85(1010):101-113.

    Not in our library10.1259/bjr/59448833

  270. 270.
    Introduction to metallic nanoparticles · 2010
    No notice
  271. 271.

    Caruso E.B., Petralia S., Conoci S., Giuffrida S., Sortino S. Photodelivery of nitric oxide from water-soluble platinum nanoparticles. J. Am. Chem. Soc. 2007;129(3):480-481.

    Not in our library10.1021/ja067568d

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    de Mel A., Chaloupka K., Malam Y., Darbyshire A., Cousins B., Seifalian A.M. A silver nanocomposite biomaterial for blood-contacting implants. J. Biomed. Mater. Res. 2012;100(9):2348-2357.

    Not in our library10.1002/jbm.a.34177

  273. 273.

    Chaloupka K., Malam Y., Seifalian A.M. Nanosilver as a new generation of nanoproduct in biomedical applications. Trends Biotechnol. 2010;28(11):580-588.

    Not in our library10.1016/j.tibtech.2010.07.006

  274. 274.

    Vittorino E., Giancane G., Manno D., Serra A., Valli L., Sortino S. Photofunctional multilayer films by assembling naked silver nanoparticles and a tailored nitric oxide photodispenser at water/air interface. J. Colloid Interface Sci. 2012;368(1):191-196.

    Not in our library10.1016/j.jcis.2011.09.084

  275. 275.

    Horcajada P., Gref R., Baati T., Allan P.K., Maurin G., Couvreur P., Férey G., Morris R.E., Serre C. Metal–organic frameworks in biomedicine. Chem. Rev. 2012;112(2):1232-1268.

    Not in our library10.1021/cr200256v

  276. 276.

    Tu Q., Zhao X., Liu S., Li X., Zhang Q., Yu H., Xiong K., Huang N., Yang Z. Spatiotemporal dual-delivery of therapeutic gas and growth factor for prevention of vascular stent thrombosis and restenosis. Applied Materials Today. 2020;19.

    Not in our library10.1016/j.apmt.2019.100546

  277. 277.

    de Vries M.R., Quax P.H.A. Inflammation in vein graft disease. Frontiers in cardiovascular medicine. 2018;5:3.

    Not in our library10.3389/fcvm.2018.00003

  278. 278.
    Dimeric Thymosin β4 Loaded Nanofibrous Interface Enhanced Regeneration of Muscular Artery in Aging Body through Modulating Perivascular Adipose Stem Cell–Macrophage Interaction · 2020
    Not checked
  279. 279.

    Wong M.M., Chen Y., Margariti A., Winkler B., Campagnolo P., Potter C., Hu Y., Xu Q. Macrophages control vascular stem/progenitor cell plasticity through tumor necrosis factor-α-mediated nuclear factor-κB activation. Arterioscler. Thromb. Vasc. Biol. 2014;34(3):635-643.

    Not in our library10.1161/atvbaha.113.302568

  280. 280.

    Liang M., Wang Y., Liang A., Dong J.F., Du J., Cheng J. Impaired integrin β3 delays endothelial cell regeneration and contributes to arteriovenous graft failure in mice. Arterioscler. Thromb. Vasc. Biol. 2015;35(3):607-615.

    Not in our library10.1161/atvbaha.114.305089

  281. 281.

    Akahori H., Karmali V., Polavarapu R., Lyle A.N., Weiss D., Shin E., Husain A., Naqvi N., Van Dam R., Habib A., Choi C.U., King A.L., Pachura K., Taylor W.R., Lefer D.J., Finn A.V. CD163 interacts with TWEAK to regulate tissue regeneration after ischaemic injury. Nat. Commun. 2015;6(1):7792.

    Not in our library10.1038/ncomms8792

  282. 282.

    Vasconcelos D.P., Costa M., Amaral I.F., Barbosa M.A., Águas A.P., Barbosa J.N. Development of an immunomodulatory biomaterial: using resolvin D1 to modulate inflammation. Biomaterials. 2015;53:566-573.

    Not in our library10.1016/j.biomaterials.2015.02.120

  283. 283.

    Sok M.C.P., Tria M.C., Olingy C.E., San Emeterio C.L., Botchwey E.A. Aspirin-Triggered Resolvin D1-modified materials promote the accumulation of pro-regenerative immune cell subsets and enhance vascular remodeling. Acta Biomater. 2017;53:109-122.

    Not in our library10.1016/j.actbio.2017.02.020

  284. 284.

    Shi J., Zhang X., Jiang L., Zhang L., Dong Y., Midgley A.C., Kong D., Wang S. Regulation of the inflammatory response by vascular grafts modified with Aspirin-Triggered Resolvin D1 promotes blood vessel regeneration. Acta Biomater. 2019;97:360-373.

    Not in our library10.1016/j.actbio.2019.07.037

  285. 285.

    Massena S., Christoffersson G., Vågesjö E., Seignez C., Gustafsson K., Binet F., Herrera Hidalgo C., Giraud A., Lomei J., Weström S., Shibuya M., Claesson-Welsh L., Gerwins P., Welsh M., Kreuger J., Phillipson M. Identification and characterization of VEGF-A–responsive neutrophils expressing CD49d, VEGFR1, and CXCR4 in mice and humans. Blood. 2015;126(17):2016-2026.

    Not in our library10.1182/blood-2015-03-631572

  286. 286.
    Nanoparticle-mediated local delivery of an antisense TGF-β1 construct inhibits intimal hyperplasia in autogenous vein grafts in rats. · 2012
    Not checked
  287. 287.

    Kalra M., Miller V.M. Early remodeling of saphenous vein grafts: proliferation, migration and apoptosis of adventitial and medial cells occur simultaneously with changes in graft diameter and blood flow. J. Vasc. Res. 2000;37(6):576-584.

    Not in our library10.1159/000054091

  288. 288.

    Mitra A.K., Gangahar D.M., Agrawal D.K. Cellular, molecular and immunological mechanisms in the pathophysiology of vein graft intimal hyperplasia. Immunol. Cell Biol. 2006;84(2):115-124.

    Not in our library10.1111/j.1440-1711.2005.01407.x

  289. 289.

    Jiang Z., Tao M., Omalley K.A., Wang D., Ozaki C.K., Berceli S.A. Established neointimal hyperplasia in vein grafts expands via TGF-beta-mediated progressive fibrosis. Am. J. Physiol. Heart Circ. Physiol. 2009;297(4):H1200-H1207.

    Not in our library10.1152/ajpheart.00268.2009

  290. 290.

    Packard R.R., Lichtman A.H., Libby P. Innate and adaptive immunity in atherosclerosis. Semin. Immunopathol. 2009;31(1):5-22.

    Not in our library10.1007/s00281-009-0153-8

  291. 291.

    Hibino N., Mejias D., Pietris N., Dean E., Yi T., Best C., Shinoka T., Breuer C. The innate immune system contributes to tissue-engineered vascular graft performance. Faseb. J. 2015;29(6):2431-2438.

    Not in our library10.1096/fj.14-268334

  292. 292.

    Ding N., Dou C., Wang Y., Liu F., Guan G., Huo D., Li Y., Yang J., Wei K., Yang M., Tan J., Zeng W., Zhu C. Antishear stress bionic carbon nanotube mesh coating with intracellular controlled drug delivery constructing small-diameter tissue-engineered vascular grafts. Adv Healthc Mater. 2018;7(11).

    Not in our library10.1002/adhm.201800026

  293. 293.

    Buttari B., Profumo E., Segoni L., D'Arcangelo D., Rossi S., Facchiano F., Saso L., Businaro R., Iuliano L., Riganò R. Resveratrol counteracts inflammation in human M1 and M2 macrophages upon challenge with 7-oxo-cholesterol: potential therapeutic implications in atherosclerosis. Oxid Med Cell Longev. 2014.

    Not in our library10.1155/2014/257543

  294. 294.

    Yang Y., Lei D., Zou H., Huang S., Yang Q., Li S., Qing F.-L., Ye X., You Z., Zhao Q. Hybrid electrospun rapamycin-loaded small-diameter decellularized vascular grafts effectively inhibit intimal hyperplasia. Acta Biomater. 2019;97:321-332.

    Not in our library10.1016/j.actbio.2019.06.037

  295. 295.

    Bessueille L., Magne D. Inflammation: a culprit for vascular calcification in atherosclerosis and diabetes. Cell. Mol. Life Sci. 2015;72(13):2475-2489.

    Not in our library10.1007/s00018-015-1876-4

  296. 296.

    Wei Y., Wu Y., Zhao R., Zhang K., Midgley A.C., Kong D., Li Z., Zhao Q. MSC-derived sEVs enhance patency and inhibit calcification of synthetic vascular grafts by immunomodulation in a rat model of hyperlipidemia. Biomaterials. 2019;204:13-24.

    Not in our library10.1016/j.biomaterials.2019.01.049

  297. 297.

    de Vries M.R., Seghers L., van Bergen J., Peters H.A.B., de Jong R.C.M., Hamming J.F., Toes R.E.M., van Hinsbergh V.W.M., Quax P.H.A. C57BL/6 NK cell gene complex is crucially involved in vascular remodeling. J. Mol. Cell. Cardiol. 2013;64:51-58.

    Not in our library10.1016/j.yjmcc.2013.08.009

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