Ubiquitin like protein FAT10 repressed cardiac fibrosis after myocardial ischemic via mediating degradation of Smad3 dependent on FAT10-proteasome system.

ABSTRACT: Cardiac fibrosis after myocardial ischemic (MI) injury is a key factor in heart function deterioration. We recently showed that ubiquitin-like protein human HLA-F adjacent transcript (FAT10) plays a novel role in ischemic cardiovascular diseases, but its function in cardiac fibrosis remains unknown. The present study aims to detail the pathophysiological function of FAT10 in MI injury-induced cardiac fibrosis and its underlying mechanism. In vivo, a systemic FAT10 deficiency mouse (Fat10 ^-/-) model was established which exhibited excessive cardiac fibrosis and deleterious cardiac function after MI when compared to wild-type mice. Cardiac fibrotic-related proteins (α-SMA, collagen I and collagen III) content were increased in MI-Fat10 ^-/- mice. Sim

SUBMITTER: Chen C 

PROVIDER: S-EPMC9910007 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature