Downregulation of circ_0001112 Enhances Myocardial Infarction Through Regulation of miR-324-5p/CDK6 Axis.

Myocardial infarction (MI) usually results in severe heart failure (HF), and patients suffer from the repercussions of MI, elucidation of the pathological basis of MI is crucial to optimize the prevention and treatment of MI. This study investigated the role of dysregulated circ_0001112 in MI. In our study, circ_0001112 was significantly upregulated in the MI model and by hypoxia treatment. Circ_0001112 overexpression inhibited hypoxia-induced cardiomyocyte apoptosis. Luciferase assay showed that circ_0001112 sponged miR-324-5p that regulated the expression of cyclin-dependent kinase 6 (CDK6). Ago2-miRNP immunoprecipitation further confirmed that the 3'-untranslated region (3'UTR) of CDK6 was targeted by miR-324-5p. Either miR-324-5p overexpression or CDK6 knockdown prevented cardiomyocyte apoptosis induced by circ_0001112 overexpression. In conclusion, this study demonstrated that the downregulation of circ_0001112 promoted cardiomyocyte apoptosis by sponging miR-324-5p and upregulating CDK6 expression in MI.