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Background  Angiotensin‐converting enzyme 3 ( ACE 3) is a recently defined homolog of  ACE . However, the pathophysiological function of  ACE 3 is largely unknown. Here, we aim to explore the role of  ACE 3 in pathological cardiac hypertrophy.    Methods and Results  Neonatal rat cardiomyocytes ( NRCM s) with gain and loss of function of  ACE 3 and mice with global knockout or cardiac‐specific overexpression of  ACE 3 were used in this study. In cultured cardiomyocytes,  ACE 3 conferred protection against angiotensin  II  (Ang  II )‐induced hypertrophic growth. Cardiac hypertrophy in mice was induced by aortic banding ( AB ) and the extent of hypertrophy was analyzed through echocardiographic, pathological, and molecular analyses. Our data demonstrated that  ACE 3‐deficient mice exhibited more pronounced cardiac hypertrophy and fibrosis and a strong decrease in cardiac contractile function, conversely, cardiac‐specific  ACE 3‐overexpressing mice displayed an attenuated hypertrophic phenotype, compared with control mice, respectively. Analyses of the underlying molecular mechanism revealed that  ACE 3‐mediated protection against cardiac hypertrophy by suppressing the activation of mitogen‐activated protein kinase kinase ( MEK )‐regulated extracellular signal‐regulated protein kinase ( ERK 1/2) signaling, which was further evidenced by the observation that inhibition of the  MEK ‐ ERK 1/2 signaling by U0126 rescued the exacerbated hypertrophic phenotype in  ACE 3‐deficient mice.    Conclusions  Our comprehensive analyses suggest that  ACE 3 inhibits pressure overload‐induced cardiac hypertrophy by blocking the  MEK ‐ ERK 1/2 signaling pathway.

Angiotensin‐Converting Enzyme 3 ( ACE 3) Protects Against Pressure Overload‐Induced Cardiac Hypertrophy