Abstract
At present, meteorin-like protein (METRNL) has been proven to be widely expressed in the myocardium and participates in the pathogenic process of various cardiovascular diseases. However, the effects of METRNL on pathological cardiac hypertrophy is still unknown. In the present study, we used a mouse model of transverse aortic constriction (TAC) surgery to mimic pathological cardiac hypertrophy and gene delivery system to overexpress METRNL in vivo. The results showed that METRNL overexpression improved TAC-induced pathological cardiac hypertrophy in mice and neonatal cardiomyocytes. In addition, METRNL overexpression diminished TAC-induced cardiac oxidative damage, inflammation and cardiomyocyte apoptosis. Moreover, the cardioprotective effect of METRNL overexpression was directly related to the activation of AMP-activated protein kinase (AMPK) and sirtuin1 (SIRT1). In summary, our data identified that METRNL may be a promising therapeutic target to mitigate pathological cardiac hypertrophy in the future.