CircTDRD3 aggravates H/R-induced cardiomyocyte apoptosis via targeting miR-4295/TP63 Axis.

The myocardial cell injury resulted from Hypoxia/Reoxygenation is the main cause of acute myocardial infarction (AMI). There're many proofs showing the functions of circRNAs in the development of AMI. The study aimed at investigating the role of circTDRD3 in myocardial injury resulted from H/R. Otherwise, the position of circTDRD3 and miR-4295 in human cardiac myocytes (HCM) apoptosis resulted from H/R were investigated. The facts that circTDRD3 was resulted from H/R injury with time and circTDRD3 knockdown could protect cardiomyocytes from H/R-regulated apoptosis were identified. More mechanism studies also unmasked that circTDRD3, acting in the place of a sponge for miR-4295, regulates TP63-dependent apoptosis. TP63 upregulation increased apoptosis resulted from H/R in primary cardiomyocytes. The circTDRD3 was established as an offbeat circRNA to regulate cardiomyocyte apoptosis, and the circTDRD3/miR-4295/TP63 axis as a mediator of cardiomyocyte apoptosis and a possible therapeutic target of service for effective treatment of cardiovascular diseases. This article is protected by copyright. All rights reserved.