{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T05:01:06Z","timestamp":1790485266401,"version":"4.1.0"},"reference-count":34,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2019,5,13]],"date-time":"2019-05-13T00:00:00Z","timestamp":1557705600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"National Natural Science Foundation of the People's Republic of China","award":["81600234"],"award-info":[{"award-number":["81600234"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2019,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Uncoupling protein 2 (UCP2), located in the mitochondrial inner membrane, is a predominant isoform of UCP that expressed in the heart and other tissues of human and rodent tissues. Nevertheless, its functional role during myocardial ischemia\/reperfusion (I\/R) is not entirely understood. Ischemic preconditioning (IPC) remarkably improved postischemic functional recovery followed by reduced lactate dehydrogenase (LDH) release with simultaneous upregulation of UCP2 in perfused myocardium. We then investigated the role of UCP2 in IPC\u2010afforded cardioprotective effects on myocardial I\/R injury with adenovirus\u2010mediated in vivo UCP2 overexpression (AdUCP2) and knockdown (AdshUCP2). IPC\u2010induced protective effects were mimicked by UCP2 overexpression, while which were abolished with silencing UCP2. Mechanistically, UCP2 overexpression significantly reinforced I\/R\u2010induced mitochondrial autophagy (mitophagy), as measured by biochemical hallmarks of mitochondrial autophagy. Moreover, primary cardiomyocytes infected with AdUCP2 increased simulated ischemia\/reperfusion (sI\/R)\u2010induced mitophagy and therefore reversed impaired mitochondrial function. Finally, suppression of mitophagy with mdivi\u20101 in cultured cardiomyocytes abolished UCP2\u2010afforded protective effect on sI\/R\u2010induced mitochondrial dysfunction and cell death. Our data identify a critical role for UCP2 against myocardial I\/R injury through preventing the mitochondrial dysfunction through reinforcing mitophagy. Our findings reveal novel mechanisms of UCP2 in the cardioprotective effects during myocardial I\/R.<\/jats:p>","DOI":"10.1002\/jcb.28812","type":"journal-article","created":{"date-parts":[[2019,5,13]],"date-time":"2019-05-13T14:36:40Z","timestamp":1557758200000},"page":"15455-15466","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":51,"title":["UCP2 protect the heart from myocardial ischemia\/reperfusion injury via induction of mitochondrial autophagy"],"prefix":"10.1002","volume":"120","author":[{"given":"Hui","family":"Wu","sequence":"first","affiliation":[{"name":"Institute of Cardiovascular Diseases China Three Gorges University Yichang Hubei China"},{"name":"Department of Cardiology Yichang Central People's Hospital Yichang Hubei China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ming","family":"Ye","sequence":"additional","affiliation":[{"name":"Institute of Cardiovascular Diseases China Three Gorges 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