Activation of ETAR and ETBR in myocardial tissue characterizes heart failure induced by experimental autoimmune myocarditis.

ABSTRACT:

Background

Endothelial dysfunction is characterized by an imbalance between endothelium-derived vasodilatory and vasoconstrictive effects and may play an important role in the development of heart failure. An increasing number of studies have shown that endothelial-derived NO-mediated vasodilation is attenuated in heart failure patients. However, the role of endothelin-1 (ET-1) in heart failure remains controversial due to its different receptors including ET-1 receptor type A (ETAR) and ET-1 receptor type B (ETBR). The aim of this study was to determine whether ET-1 and its receptors are activated and to explore the role of ETAR and ETBR in heart failure induced by myocarditis.

Methods

We constructed an animal model of experimental autoimmune myocarditis (EAM) with porcine

SUBMITTER: Yang P 

PROVIDER: S-EPMC10763419 | biostudies-literature | 2024 Jan

REPOSITORIES: biostudies-literature