LAUSR

Heart often undergoes mal-remodeling and hypertrophic growth in response to pathological stress. MiRNAs can regulate the cardiac function and participate in the regulation of cardiac hypertrophy. The present study aims at identifying the role of miR-296-5p in cardiac hypertrophy and further the underlying mechanism in hypertrophic cascades. Mice with cardiac hypertrophy were established by transverse aortic constriction (TAC). Cardiac hypertrophy in cardiomyocytes was induced by angiotensin II. Expression of miR-296-5p and its target gene CACNG6 was examined in cardiomyocytes transfected by miRNA. The expression of miR-296-5p was upregulated in mice with TAC surgery. The inhibition of miR-296-5p attenuated cardiac hypertrophy both in vitro and in vivo. And dual-luciferase reporter assays showed CACNG6 was the direct target of miR-296-5p, which modulated the expression of calcium signaling. MiR-296-5p was found to aggravate cardiac hypertrophy by targeting CACNG6, which suggests inhibition of miR-296-5p might have clinical potential to suppress cardiac hypertrophy and heart failure.