{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T19:39:59Z","timestamp":1792093199142,"version":"4.4.0"},"reference-count":41,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2020,1,22]],"date-time":"2020-01-22T00:00:00Z","timestamp":1579651200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["U1704167"],"award-info":[{"award-number":["U1704167"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2020,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Cardiomyocyte apoptosis induced by hypoxia and ischemia plays important roles in heart dysfunction after acute myocardial infarction (AMI). However, the mechanism of apoptosis induction remains unclear. A previous study reported that Y\u2010box protein 1 (YB1) is upregulated after myocardial hypoxia\/reoxygenation or ischemia\/reperfusion (H\/R or I\/R, respectively) injury; however, whether YB1 is associated with H\/R\u2010induced cardiomyocyte apoptosis is completely unknown. In the present study, we investigated the roles of YB1 in H\/R\u2010induced cardiomyocyte apoptosis and the possible underlying molecular mechanisms. In vitro, H\/R treatment upregulated the YB1 expression in H9C2 cells, whereas YB1 knockdown inhibited H\/R\u2010induced cardiomyocyte apoptosis and induced H9C2 cell proliferation via Src homology region 2 domain\u2010containing phosphatase 1 (SHP\u20101)\u2010mediated activation of signal transducer and activator of transcription 3 (STAT3). In vivo, YB1 knockdown ameliorated AMI, reducing infarct size, cardiomyocyte apoptosis,\u00a0and oxidative stress, via SHP\u20101\u2010mediated inactivation of STAT3. Additionally, YB1 knockdown inhibited H\/R\u2010 or I\/R\u2010induced oxidative stress in vitro and in vivo. H\/R and I\/R increase YB1 expression, and YB1 knockdown ameliorates AMI injury via SHP\u20101\u2010dependent STAT3 inactivation.<\/jats:p>","DOI":"10.1002\/jcp.29474","type":"journal-article","created":{"date-parts":[[2020,1,22]],"date-time":"2020-01-22T10:38:40Z","timestamp":1579689520000},"page":"8187-8198","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Y\u2010box protein 1 promotes hypoxia\/reoxygenation\u2010 or ischemia\/reperfusion\u2010induced cardiomyocyte apoptosis via SHP\u20101\u2010dependent STAT3 inactivation"],"prefix":"10.1002","volume":"235","author":[{"given":"Xueming","family":"Cao","sequence":"first","affiliation":[{"name":"Department of Cardiology, Henan Provincial Key Lab For Control of Coronary Heart Disease, Heart Center of Henan Provincial People's Hospital, Central China Fuwai Hospital Central China Fuwai Hospital of Zhengzhou University Zhengzhou 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