The case for FAT10 as a novel target in fatty liver diseases
Madushika M. Wimalarathne, Quiana C. Wilkerson-Vidal, Emily C. Hunt and 1 more
Frontiers in Pharmacology · 2022
doi:10.3389/fphar.2022.972320 (opens in a new tab)
We email you when a new notice or a question about this paper appears.
Abstract
Human leukocyte antigen F locus adjacent transcript 10 (FAT10) is a ubiquitin-like protein that targets proteins for degradation. TNFα and IFNγ upregulate FAT10, which increases susceptibility to inflammation-driven diseases like nonalcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), and hepatocellular carcinoma (HCC). It is well established that inflammation contributes to fatty liver disease, but how inflammation contributes to upregulation and what genes are involved is still poorly understood. New evidence shows that FAT10 plays a role in mitophagy, autophagy, insulin signaling, insulin resistance, and inflammation which may be directly associated with fatty liver disease development. This review will summarize the current literature regarding FAT10 role in developing liver diseases and potential therapeutic targets for nonalcoholic/alcoholic fatty liver disease and hepatocellular carcinoma.
Abstract licence: CC BY
References111
- 30.
39 more references, whose wording the paper’s licence keeps private.
All 111 referencesReads
Read by people on this page
None yet.
Checked or read by AI through naulon
None yet.
A person counts once a day per paper. We keep no cookie and no address: a reader is a hash that changes every day. Any month under five reads shows no number.
Are you an author?
Is this your paper?
Claim it to add your note and be paid when agents cite it. Free.