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In this study, mitochondrial biogenesis was markedly impaired induced by high glucose (HG), as evidenced by dysregulated mitochondrial structure, reduced mitochondrial DNA contents, and biogenesis\u2010related mRNA levels, accompanied by increased cell apoptosis. MiR\u2010144 was identified to be decreased in HG\u2010induced cardiomyocytes and in streptozotocin (STZ)\u2010challenged heart samples. Forced miR\u2010144 expression enhanced mitochondrial biogenesis and suppressed cell apoptosis, while miR\u2010144 inhibition exhibited the opposite results. Rac\u20101 was identified as a target gene of miR\u2010144. Decreased Rac\u20101 levels activated AMPK phosphorylation and PGC\u20101\u03b1 deacetylation, leading to increased mitochondrial biogenesis and reduced cell apoptosis. Importantly, the systemic neutralization of miR\u2010144 attenuated mitochondrial disorder and ventricular dysfunction following STZ treatment. Additionally, plasma miR\u2010144 decreased markedly in diabetic patients with cardiac dysfunction. The receiver\u2010operator characteristic curve showed that plasma miR\u2010144 could specifically predict diabetic patients developing cardiac dysfunction. In conclusion, this study provides strong evidence suggesting that miR\u2010144 protects heart from hyperglycemia\u2010induced injury by improving mitochondrial biogenesis and decreasing cell apoptosis\n                    <jats:italic>via<\/jats:italic>\n                    targeting Rac\u20101. Forced miR\u2010144 expression might, thus, be a protective strategy for treating hyperglycemia\u2010induced cardiac dysfunction.\n                  <\/jats:p>","DOI":"10.1096\/fj.201901838r","type":"journal-article","created":{"date-parts":[[2019,12,13]],"date-time":"2019-12-13T01:10:45Z","timestamp":1576199445000},"page":"2173-2197","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":50,"title":["MiR\u2010144 protects the heart from hyperglycemia\u2010induced injury by regulating mitochondrial biogenesis and cardiomyocyte apoptosis"],"prefix":"10.1096","volume":"34","author":[{"given":"Lichan","family":"Tao","sequence":"first","affiliation":[{"name":"Department of Cardiology The Third Affiliated Hospital of Soochow University Changzhou City China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoli","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Endocrinology The Third 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