Overexpression of microRNA-138 attenuates cardiac hypertrophic response through repression of YAP1

MicroRNAs (miRNAs) have been identified as important players in the pathogenesis of cardiac hypertrophy. In the present study, we evaluated the potential role of miR-138 in cardiac hypertrophy and the potential molecular mechanisms. We observed that in mice with transverse aortic constriction (TAC), miR-138 expression was remarkably reduced in the hypertrophic hearts. Overexpression of miR-138 attenuated the cardiac hypertrophy in vivo and the hypertrophic responses in Ang-II-treated mouse cardiomyocytes in vitro. YAP1 was experimentally validated as a direct target of miR-138, and its mRNA and protein levels were increased in Ang-II-treated cardiomyocytes. Therefore, the findings of the present article revealed a novel molecular mechanism for cardiac hypertrophy and indicated miR-138 as a potential therapeutic target for this disease.