{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,29]],"date-time":"2026-07-29T17:03:42Z","timestamp":1785344622300,"version":"3.55.0"},"reference-count":41,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2020,11,20]],"date-time":"2020-11-20T00:00:00Z","timestamp":1605830400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["iubmb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["IUBMB Life"],"published-print":{"date-parts":[[2020,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>Over the years, the roles of microRNAs (miRNAs) and histone deacetylase 3 (HDAC3) in human diseases have been investigated. This study focused on the effect of miR\u201019a\u20103p and HDAC3 in myocardial ischemia\u2013reperfusion (I\/R) injury (MIRI) by targeting cyclin\u2010dependent kinase 2 (CDK2).<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>The I\/R rat models were established by coronary artery ligation, which were then treated with RGFP966 (an inhibitor of HDAC3), miR\u201019a\u20103p agomir or antagomir, or silenced CDK2 to explore their roles in the cardiac function, pathological changes of myocardial tissues, myocardial infarction area, inflammatory factors and oxidative stress factors in rats with MIRI. The expression of miR\u201019a\u20103p, HDAC3, and CDK2 was determined by RT\u2010qPCR and western blot assay, and the interaction among which was also verified by online prediction, luciferase activity assay and ChIP assay.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The results indicated that HDAC3 and CDK2 were upregulated while miR\u201019a\u20103p was downregulated in myocardial tissues of I\/R rats. The inhibited HDAC3\/CDK2 or elevated miR\u201019a\u20103p could promote cardiac function, attenuate pathological changes, inflammatory reaction, oxidative stress, myocardial infarction area and apoptosis of myocardial tissues. HDAC3 mediates miR\u201019a\u20103p and CDK2 is targeted by miR\u201019a\u20103p.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Inhibited HDAC3 ameliorates MIRI in a rat model by elevating miR\u201019a\u20103p and reducing CDK2, which may contribute to the treatment of MIRI.<\/jats:p><\/jats:sec>","DOI":"10.1002\/iub.2402","type":"journal-article","created":{"date-parts":[[2020,11,21]],"date-time":"2020-11-21T02:52:18Z","timestamp":1605927138000},"page":"2696-2709","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Inhibited histone deacetylase 3 ameliorates myocardial ischemia\u2013reperfusion injury in a rat model by elevating <scp>microRNA<\/scp>\u201019a\u20103p and reducing cyclin\u2010dependent kinase 2"],"prefix":"10.1002","volume":"72","author":[{"given":"Kaiyou","family":"Song","sequence":"first","affiliation":[{"name":"Cardiovascular Department Linyi People's Hospital  Linyi 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