Decreased autophagy induced by β₁-adrenoceptor autoantibodies contributes to cardiomyocyte apoptosis.

ABSTRACT: It has been recognized that myocardial apoptosis is one major factor in the development of heart dysfunction and autophagy has been shown to influence the apoptosis. In previous studies, we reported that anti-β₁-adrenergic receptor autoantibodies (β₁-AABs) decreased myocardial autophagy, but the role of decreased autophagy in cardiomyocyte apoptosis remains unclear. In the present study, we used a β₁-AAB-immunized rat model to investigate the role of decreased autophagy in cardiomyocyte apoptosis. We reported that the level of autophagic flux increased early and then decreased in an actively β₁-AAB-immunized rat model. Rapamycin, an mTOR inhibitor, restored myocardial apoptosis in the presence of β₁-AABs. Further, we found that the ear

SUBMITTER: Wang L 

PROVIDER: S-EPMC5852148 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature