inhibits isoproterenol-induced cardiac hypertrophy by targetting c-Jun.

Hypertrophic cardiomyopathy (HCM) is a serious monogenic disease characterized by cardiac hypertrophy, fibrosis, sudden cardiac death, and heart failure. Previously, we identified that was down-regulated in HCM patients. However, the regulatory effects of remain unclear. Thus, we investigated the role of in the regulation of cardiac hypertrophy. The expression of in left ventricular tissues in HCM patients and mice subjected to transverse aortic constriction (TAC) was significantly down-regulated. Knockdown of expression in neonatal rat cardiomyocytes (NRCMs) induced cardiomyocyte enlargement and increased atrial natriuretic polypeptide (ANP) expression. Overexpression of antagonized isoproterenol (ISO)-induced cardiomyocyte enlargement and ANP/brain natriuretic peptide (BNP) up-regulation. More importantly, we found that c-Jun expression was inhibited by in NRCMs. Knockdown of c-Jun expression significantly attenuated cardiac hypertrophy induced by deprivation. Our data indicated that was down-regulated in the hearts of HCM patients and that it inhibited cardiac hypertrophy by targetting c-Jun expression.