myocardial ischemia-reperfusion

[Cell Biology International] Researchers showed that methyltransferase-like 3 (METTL3) was downregulated in mice ischemia-reperfusion (I/R) myocardial tissues and hypoxic/re-oxygenated (H/R) cardiomyocytes, and upregulation of METTL3 attenuated I/R and H/R-induced cell apoptosis.

[Cell Death Discovery] Investigators defined the underlying role of histone deacetylase 4 (HDAC4) and miR-206 in the pathological process of myocardial ischemia-reperfusion injury (MIRI). Up-regulation of HDAC4 and down-regulation of miR-206 occurred in rat myocardial tissues and cardiomyocytes in MIRI.

[Acta Pharmacologica Sinica] Scientists investigated the role of lncRNAs in myocardial ischemia-reperfusion injury. Overexpression of p53 canceled the inhibitory effects of lncRNA-6395 knockdown on cardiomyocyte apoptosis, whereas knockdown of p53 counteracted the apoptotic effects of lncRNA-6395 in cardiomyocytes.

[Cell Death & Disease] Ischemia/reperfusion (IR) injury mice with myocardial overexpression GDF11 exhibited a significantly smaller myocardial infarct size, less cardiac remodeling and dysfunction, fewer apoptotic cardiomyocytes, higher telomerase activity, longer telomeres, and higher ATP generation than IR mice treated with an adenovirus carrying a negative control plasmid.

[Journal of Molecular Histology] In vitro, neonatal ventricle cardiomyocyte hypoxia/reoxygenation model was constructed to mimic myocardial ischemia/reperfusion. PSMB4 silence promoted cardiomyocyte apoptosis and IκBα expression, inhibited the activation of NF-κB.

[Cell Death Discovery] The authors examined the regulatory effect of circular RNA HIPK3 (circHIPK3) during myocardial ischemia/reperfusion and investigated its mechanism in cardiomyocyte autophagy and apoptosis.