{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,4]],"date-time":"2026-06-04T16:30:39Z","timestamp":1780590639121,"version":"3.54.1"},"reference-count":30,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2022,1,25]],"date-time":"2022-01-25T00:00:00Z","timestamp":1643068800000},"content-version":"vor","delay-in-days":24,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100004608","name":"Natural Science Foundation of Jiangsu Province","doi-asserted-by":"publisher","award":["BE2021735"],"award-info":[{"award-number":["BE2021735"]}],"id":[{"id":"10.13039\/501100004608","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004608","name":"Natural Science Foundation of Jiangsu Province","doi-asserted-by":"publisher","award":["BK20190352"],"award-info":[{"award-number":["BK20190352"]}],"id":[{"id":"10.13039\/501100004608","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":[[2022,1]]},"abstract":"<jats:p><jats:italic>Objective<\/jats:italic>. Myocardial ischemia\/reperfusion (I\/R) injury can aggravate myocardial injury. Programmed necrosis plays a crucial role in this injury. However, the role of exosomal miRNAs in myocardial I\/R injury remains unclear. Therefore, this study is aimed at exploring the function and mechanism of exosomal miR\u201017\u20103p in myocardial I\/R injury. <jats:italic>Methods<\/jats:italic>. The myocardial I\/R injury animal model was established in C57BL\/6 mice. Exosomes were identified using transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and Western blotting. Programmed necrosis was detected by PI staining. Heart function and myocardial infarct size were evaluated using echocardiography and triphenyl tetrazolium chloride (TTC) staining, respectively. Histopathological changes were visualized by hematoxylin and eosin (H&amp;E) and Masson staining. The regulation of TIMP3 expression by miR\u201017\u20103p was verified using a dual\u2010luciferase reporter assay. Lactate dehydrogenase (LDH) and tumor necrosis factor\u2010<jats:italic>\u03b1<\/jats:italic> (TNF\u2010<jats:italic>\u03b1<\/jats:italic>) levels were measured by enzyme\u2010linked immunosorbent assays (ELISA). TIMP3 expression was measured by quantitative reverse transcription\u2010polymerase chain reaction (qRT\u2010PCR) and Western blotting. <jats:italic>Results<\/jats:italic>. We demonstrated that miR\u201017\u20103p was significantly downregulated in peripheral blood exosomes after cardiac I\/R injury. Further analysis indicated that exosomal miR\u201017\u20103p attenuated H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>\u2010induced programmed necrosis in cardiomyocytes in vitro. Moreover, TIMP3 was a target for miR\u201017\u20103p. TIMP3 affected H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>\u2010induced programmed necrosis in cardiomyocytes. This effect was modulated by miR\u201017\u20103p in vitro. Furthermore, exosomal miR\u201017\u20103p greatly alleviated cardiac I\/R injury in vivo. <jats:italic>Conclusions<\/jats:italic>. The present study demonstrated that exosomal miR\u201017\u20103p alleviated the programmed necrosis associated with cardiac I\/R injury by regulating TIMP3 expression. These findings could represent a potential treatment for I\/R injury.<\/jats:p>","DOI":"10.1155\/2022\/2785113","type":"journal-article","created":{"date-parts":[[2022,1,25]],"date-time":"2022-01-25T21:20:06Z","timestamp":1643145606000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Exosomal miR\u201017\u20103p Alleviates Programmed Necrosis in Cardiac Ischemia\/Reperfusion Injury by Regulating TIMP3 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