lncRNA HAGLR modulates myocardial ischemia-reperfusion injury in mice through regulating miR-133a-3p/MAPK1 axis.

Abstract

Acute myocardial infarction is one of the leading causes of morbidity worldwide, but the underlying mechanism responsible for myocardial ischemia-reperfusion (I/R) injury remains elusive. lncRNA plays roles in inflammatory response, cell apoptosis and regulation of myocardial ischemia. However, whether lncRNA HAGLR could regulate myocardial I/R injury and the molecular mechanism need to be further investigated. lncRNA has been shown to bind to miRNAs and compete with endogenous RNAs. miR-133a-3p has been shown to regulate cardiomyocyte apoptosis and ischemic myocardial injury. In this work, it has shown that knockdown of HAGLR could suppress inflammatory response and cell apoptosis induced by I/R and, thus, alleviate myocardial I/R injury. HAGLR promoted myocardial I/R injury by inhibiting miR-133a-3p to promote MAPK1 expression.

• Authors: Zi Wang, Wenqi Luo, Peng Zhong, Yifan Feng, Huaibin Wang
• Journal: Open medicine (Warsaw, Poland) (Open Med (Wars)) Vol. 17 Issue 1 Pg. 1299-1307 ( 2022) ISSN: 2391-5463 [Print] Poland
• PMID: 35937000 (Publication Type: Journal Article)
• Copyright: © 2022 Zi Wang et al., published by De Gruyter.