{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T14:58:47Z","timestamp":1787065127980,"version":"build-2736575974"},"reference-count":51,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2019,10,20]],"date-time":"2019-10-20T00:00:00Z","timestamp":1571529600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2019,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Mounting evidence has indicated that long non\u2010coding RNA maternally expressed gene 3 (lncRNA MEG3) regulates cell apoptosis, and is involved in a variety of diseases. However, its exact role in myocardial infarction (MI) has not been fully elucidated. In the present study, we firstly observed that the expression levels of the lncRNA MEG3 in infarct hearts and hypoxic neonatal mice ventricular myocytes (NMVMs) were up\u2010regulated by quantitative real\u2010time PCR (qRT\u2010PCR). Then, we knocked down lncRNA MEG3 by lentiviral delivery in the myocardial border region following multipoint injection. Following 28\u00a0days of MI, the lncRNA MEG3 knockdown mice indicated better cardiac function, and less cardiac remodelling by ultrasonic cardiogram and histological analysis. In addition, we indicated that lncRNA MEG3 knockdown reduced myocyte apoptosis and reactive oxygen species production in MI mice model and hypoxic NMVMs. Furthermore, we revealed that knockdown of lncRNA MEG3 protected against endoplasmic reticulum stress (ERS)\u2010mediated myocardial apoptosis including the induction of PERK\u2010eIF2\u03b1 and caspase 12 pathways. At last, we provided evidence that p53 was identified as a protein target of lncRNA MEG3 to regulate NF\u2010\u03baB\u2010 and ERS\u2010associated apoptosis. Taken collectively, our findings demonstrated that lncRNA MEG3 knockdown exerted cardioprotection by reducing ERS\u2010mediated apoptosis through targeting p53 post\u2010MI.<\/jats:p>","DOI":"10.1111\/jcmm.14714","type":"journal-article","created":{"date-parts":[[2019,10,20]],"date-time":"2019-10-20T21:46:07Z","timestamp":1571607967000},"page":"8369-8380","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":38,"title":["Long non\u2010coding RNA MEG3 knockdown attenuates endoplasmic reticulum stress\u2010mediated apoptosis by targeting p53 following myocardial infarction"],"prefix":"10.1111","volume":"23","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3975-6860","authenticated-orcid":false,"given":"Xueling","family":"Li","sequence":"first","affiliation":[{"name":"Department of Cardiology Zhejiang provincial People\u2019s Hospital People\u2019s Hospital of Hangzhou Medical College Hangzhou China"},{"name":"Department of 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