title: Mitochondrial autophagy in cardiomyopathy.
abstract: Cardiac mitochondria produce vast amounts of ATP through oxidative phosphorylation to maintain contractile function. They are also the primary source of reactive oxygen species, which contribute to mitochondrial dysfunction, cardiomyocyte death, and heart failure. To protect against mitochondrial damage, cardiomyocytes develop well-coordinated quality control mechanisms that maintain the overall mitochondrial health through mitochondrial biogenesis, mitochondrial dynamics, and mitochondrial autophagy (mitophagy). Mitophagy removes dysfunctional mitochondria in the heart not only under normal physiological conditions, but also in response to pathological stresses. Accumulating evidence suggests that mitophagy dysregulation can induce cardiomyocyte death and cardiomyopathy. In this review, we discuss what is currently known about mitophagic mechanisms, regulatory pathways, and function in the heart.
authors.affiliation: Department of Cell Biology and Molecular Medicine, Rutgers - New Jersey Medical School, USA.
authors.forename: Mingming
authors.initials: M
authors.lastname: Tong
authors.affiliation: Department of Cell Biology and Molecular Medicine, Rutgers - New Jersey Medical School, USA. Electronic address: sadoshju@njms.rutgers.edu.
authors.forename: Junichi
authors.initials: J
authors.lastname: Sadoshima
mesh_terms: D009202:Cardiomyopathies / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D008929:Mitochondria, Heart / Q000235:genetics* / Q000378:metabolism; D063306:Mitophagy / Q000235:genetics*; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology; D010085:Oxidative Phosphorylation; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D017382:Reactive Oxygen Species