{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,2]],"date-time":"2025-12-02T03:16:56Z","timestamp":1764645416967,"version":"3.37.3"},"reference-count":36,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["No.XP","81460047","No.XP","81660359"],"award-info":[{"award-number":["No.XP","81460047","No.XP","81660359"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Cell Physiology"],"published-print":{"date-parts":[[2019,8,1]]},"abstract":"<jats:p> Myocardial ischemia-reperfusion (I\/R) is a common and lethal disease that threatens people\u2019s life worldwide. The underlying mechanisms are under intensive study and yet remain unclear. Here, we explored the function of miR-322\/503 in myocardial I\/R injury. We used isolated rat perfused heart as an in vivo model and H9c2 cells subjected with the oxygen and glucose deprivation followed by reperfusion as in vitro model to study myocardial I\/R injury. 2,3,5-Triphenyltetrazolium chloride (TTC) staining was used to measure the infarct size, and terminal deoxynucleotidyl transferase dUTP-mediated nick-end label (TUNEL) staining was used to examine apoptosis. Quantitative RT-PCR and Western blot were used to determine expression levels of miR-322\/503, Smad ubiquitin regulatory factor 2 (Smurf2), enhancer of zeste homolog 2 (EZH2), p-Akt, and p-GSK3\u03b2. Overexpression of miR-322\/503 decreased infarct size, inhibited cell apoptosis, and promoted cell proliferation through upregualtion of p-Akt and p-GSK3\u03b2. Thus the expression of miR-322\/503 was reduced during I\/R process. On the molecular level, miR-322\/503 directly bound Smurf2 mRNA and suppressed its translation. Smurf2 ubiquitinated EZH2 and degraded EZH2, which could activate Akt\/GSK3\u03b2 signaling. Our study demonstrates that miR-322\/503 plays a beneficial role in myocardial I\/R injury. By inhibition of Smurf2 translation, miR-322\/503 induces EZH2 expression and activates Akt\/GSK3\u03b2 pathway, thereby protecting cells from ischemia reperfusion injury. <\/jats:p>","DOI":"10.1152\/ajpcell.00375.2018","type":"journal-article","created":{"date-parts":[[2019,1,16]],"date-time":"2019-01-16T20:05:50Z","timestamp":1547669150000},"page":"C253-C261","source":"Crossref","is-referenced-by-count":31,"title":["Inhibition of Smurf2 translation by miR-322\/503 protects from ischemia-reperfusion injury by modulating EZH2\/Akt\/GSK3\u03b2 signaling"],"prefix":"10.1152","volume":"317","author":[{"given":"Wei","family":"Dong","sequence":"first","affiliation":[{"name":"Department of Cardiovascular, The First Affiliated Hospital of Nanchang University, Nanchang, People\u2019s Republic of China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fei","family":"Xie","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular, The First Affiliated Hospital of 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