Exercise reestablishes autophagic flux and mitochondrial quality control in heart failure.

ABSTRACT: We previously reported that facilitating the clearance of damaged mitochondria through macroautophagy/autophagy protects against acute myocardial infarction. Here we characterize the impact of exercise, a safe strategy against cardiovascular disease, on cardiac autophagy and its contribution to mitochondrial quality control, bioenergetics and oxidative damage in a post-myocardial infarction-induced heart failure animal model. We found that failing hearts displayed reduced autophagic flux depicted by accumulation of autophagy-related markers and loss of responsiveness to chloroquine treatment at 4 and 12 wk after myocardial infarction. These changes were accompanied by accumulation of fragmented mitochondria with reduced O₂ consumption, elevated H₂O₂ release

SUBMITTER: Campos JC 

PROVIDER: S-EPMC5584854 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature