{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["19(3)"],"submitter":["Chen C"],"pubmed_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. <i>In vivo</i>, a systemic FAT10 deficiency mouse (<i>Fat10</i> <sup>-/-</sup>) 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-<i>Fat10</i> <sup>-/-</sup> mice. Sim"],"journal":["International journal of biological sciences"],"pagination":["881-896"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9910007"],"repository":["biostudies-literature"],"pubmed_title":["Ubiquitin like protein FAT10 repressed cardiac fibrosis after myocardial ischemic via mediating degradation of Smad3 dependent on FAT10-proteasome system."],"pmcid":["PMC9910007"],"pubmed_authors":["Li X","Wan R","Yu B","Xie J","Hong K","Zhou T","Chen C","Su Y","Shen Y","Jin J"],"additional_accession":[]},"is_claimable":false,"name":"Ubiquitin like protein FAT10 repressed cardiac fibrosis after myocardial ischemic via mediating degradation of Smad3 dependent on FAT10-proteasome system.","description":"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. <i>In vivo</i>, a systemic FAT10 deficiency mouse (<i>Fat10</i> <sup>-/-</sup>) 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-<i>Fat10</i> <sup>-/-</sup> mice. Sim","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023","modification":"2025-05-29T16:30:18.856Z","creation":"2025-04-04T23:57:09.059Z"},"accession":"S-EPMC9910007","cross_references":{"pubmed":["36778114"],"doi":["10.7150/ijbs.77677"]}}