Apelin-13 protects against myocardial infarction-induced myocardial fibrosis

Abstract

Myocardial infarction is a serious health threat. Apelin is an endogenous ligand of angiotensin II receptor-like 1 (APJ) and the apelin/APJ system is associated with various types of heart disease. However, whether apelin protects against myocardial infarction-induced myocardial fibrosis remains unclear. The present study aimed to investigate the function of apelin-13 during myocardial infarction-induced myocardial fibrosis, and to determine the mechanism underlying the effects of apelin-13. Apelin-13 was demonstrated to improve left ventricular function and results of hematoxylin and eosin staining, Masson's trichrome staining and western blotting showed that apelin-13 attenuated myocardial fibrosis. Further mechanistic investigation was performed by enzyme-linked immunosorbent assay, western blotting and electrophoretic mobility shift assay. The results demonstrated that apelin-13 inhibited the activation of nuclear factor (NF)-κB signaling in vitro and in vivo. To the best of our knowledge, the present study was the first to demonstrate that apelin-13 may attenuate myocardial infarction-induced myocardial fibrosis, and that this protective function may be mediated by inhibition of NF-κB signaling. The present study suggests a theoretical basis for the effects of apelin-13 and provides insight into the potential clinical application of apelin-13.