{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T12:42:57Z","timestamp":1791981777871,"version":"4.4.0"},"reference-count":52,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2021,6,30]],"date-time":"2021-06-30T00:00:00Z","timestamp":1625011200000},"content-version":"vor","delay-in-days":180,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81900338"],"award-info":[{"award-number":["81900338"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Oxidative Medicine and Cellular Longevity"],"published-print":{"date-parts":[[2021,1]]},"abstract":"<jats:p>\n                    <jats:italic>Background<\/jats:italic>\n                    . miR\u2010205 is important for oxidative stress, mitochondrial dysfunction, and apoptosis. The roles of miR\u2010205 in cardiac ischemia\/reperfusion (I\/R) injury remain unknown. The aim of this research is to reveal whether miR\u2010205 could regulate cardiac I\/R injury by focusing upon the oxidative stress, mitochondrial function, and apoptosis.\n                    <jats:italic>Methods<\/jats:italic>\n                    . Levels of miR\u2010205 and Rnd3 were examined in the hearts with I\/R injury. Myocardial infarct size, cardiac function, oxidative stress, mitochondria function, and cardiomyocyte apoptosis were detected in mice with myocardial ischemia\/reperfusion (MI\/R) injury. The primary neonatal cardiomyocytes underwent hypoxia\/reoxygenation (H\/R) to simulate MI\/R injury.\n                    <jats:italic>Results<\/jats:italic>\n                    . miR\u2010205 levels were significantly elevated in cardiac tissues from I\/R in comparison with those from Sham. In comparison with controls, levels of Rnd3 were significantly decreased in the hearts from mice with MI\/R injury. Furthermore, inhibiting miR\u2010205 alleviated MI\/R\u2010induced apoptosis, reduced infarct size, prevented oxidative stress increase and mitochondrial fragmentation, and improved mitochondrial functional capacity and cardiac function. Consistently, overexpression of miR\u2010205 increased infarct size and promoted apoptosis, oxidative stress, and mitochondrial dysfunction in mice with MI\/R injury. In cultured mouse neonatal cardiomyocytes, downregulation of miR\u2010205 reduced oxidative stress in H\/R\u2010treated cardiomyocytes. Finally, inhibiting Rnd3 ablated the cardioprotective effects of miR\u2010205 inhibitor in MI\/R injury.\n                    <jats:italic>Conclusions<\/jats:italic>\n                    . We conclude that inhibiting miR\u2010205 reduces infarct size, improves cardiac function, and suppresses oxidative stress, mitochondrial dysfunction, and apoptosis by promoting Rnd3 in MI\/R injury. miR\u2010205 inhibitor\u2010induced Rnd3 activation is a valid target to treat MI\/R injury.\n                  <\/jats:p>","DOI":"10.1155\/2021\/9986506","type":"journal-article","created":{"date-parts":[[2021,6,30]],"date-time":"2021-06-30T16:05:27Z","timestamp":1625069127000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":20,"title":["Inhibiting miR\u2010205 Alleviates Cardiac Ischemia\/Reperfusion Injury by Regulating Oxidative Stress, Mitochondrial Function, and 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