Cardiovascular disease is associated with declines in mitochondrial function, which can result from changes in mitochondrial abundance and metabolic activity as well as reversible and irreversible damage to mitochondrial proteins and mitochondrial DNA (mtDNA). Autophagy, a lysosomal-mediated process of protein degradation, is emerging as a prominent mediator of cardiac remodeling in the failing heart. Experiments are ongoing to determine the role of selective degradation of mitochondria (mitophagy) in heart failure and identify mechanisms that regulate this process.
