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