Overexpression of microRNA-26b attenuates angiotensin II-induced cardiac hypertrophy through inhibition of autophagic responses.

Although microRNA-26b (miR-26b) has been previously identified as a regulator of cardiac hypertrophy, the specific mechanism remains elusive. Cardiac hypertrophy was induced by thoracic aortic constriction (TAC) in mice. Four weeks after surgery, the cardiac hypertrophy mice model was successfully established. In addition, a cell model of hypertrophy was also established based on angiotensin II (AngII)-induced neonatal mouse ventricular cardiomyocytes. We observed that miR-26b was markedly down-regulated in hypertrophic myocardium tissues and hypertrophic cultured cardiomyocytes, whereas administration of miR-26b mimics suppressed hypertrophic phenotype of cultured cardiomyocytes. Additionally, it was shown that overexpression of miR-26b attenuated autophagic responses in hypertrophic cardiomyocytes, which was confirmed by reducing Beclin-1 expression and the light chain 3(LC3)-II/LC3-I ratio. Taken together, our study provides substantial evidence that upregulation of miR-26b expression might be a potential effective therapeutic strategy to attenuate cardiac hypertrophy.