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Although microRNAs have been the focus of many studies on cardiac apoptosis and fibrosis in MI, the detailed effects of miR\u201026a is needed to further understood. The present study demonstrated that miR\u201026a was downregulated in ST\u2010elevation MI (STEMI) patients and oxygen\u2010glucose deprivation (OGD)\u2010treated H9c2 cells. Downregulation of miR\u201026a was closely correlated with the increased expression of creatine kinase, creatine kinase\u2010MB and troponin I in STEMI patients. Further analysis identified that ataxia\u2013telangiectasia mutated (ATM) was a target gene for miR\u201026a based on a bioinformatics analysis. miR\u201026a overexpression effectively reduced ATM expression, apoptosis, and apoptosis\u2010related proteins in OGD\u2010treated H9c2 cells. In a mouse model of MI, the expression of miR\u201026a was significantly decreased in the infarct zone of the heart, whereas apoptosis and ATM expression were increased. miR\u201026a overexpression effectively reduced ATM expression and cardiac apoptosis at Day 1 after MI. Furthermore, we demonstrated that overexpression of miR\u201026a improved cardiac function and reduced cardiac fibrosis by the reduced expression of collagen type I and connective tissue growth factor (CTGF) in mice at Day 14 after MI. Overexpression of miR\u201026a or ATM knockdown decreased collagen I and CTGF expression in cultured OGD\u2010treated cardiomyocytes. Taken together, these data demonstrate a prominent role for miR\u201026a in linking ATM expression to ischemia\u2010induced apoptosis and fibrosis, key features of MI progression. miR\u201026a reduced MI development by affecting ATM expression and could be targeted in the treatment of MI.<\/jats:p>","DOI":"10.1002\/jcp.29537","type":"journal-article","created":{"date-parts":[[2020,1,28]],"date-time":"2020-01-28T12:15:03Z","timestamp":1580213703000},"page":"6085-6102","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":41,"title":["miR\u201026a attenuates cardiac apoptosis and fibrosis by targeting ataxia\u2013telangiectasia mutated in myocardial infarction"],"prefix":"10.1002","volume":"235","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6239-2255","authenticated-orcid":false,"given":"Ming\u2010Hsien","family":"Chiang","sequence":"first","affiliation":[{"name":"Department of Anatomy and Cell Biology, College of Medicine 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