title: Parkin-dependent mitophagy in the heart.
abstract: Mitochondria can undergo autophagic elimination for differing reasons, e.g. as part of a cell-wide macroautophagic response, as part of mitochondrial turnover during metabolic remodeling, or in the case of selective mitophagic destruction of dysfunctional mitochondria, during mitochondrial quality control. Multiple mechanistically distinct pathways converge upon, and activate, mitochondrial autophagy. Here, the evidence supporting a role for the prototypical mitochondrial quality control pathway, PINK1-Parkin mediated mitophagy, in cardiac homeostasis and heart disease is reviewed. Contrary to popular wisdom based on findings from non-cardiac systems, current data do not support a major role for Parkin-mediated mitophagy as a mechanism for constitutive mitochondrial housekeeping, and instead suggest that this pathway primarily functions in adult hearts as an inducible cardiac stress-response mechanism. Recent findings have also uncovered an unsuspected role for Parkin-mediated mitochondrial turnover in the normal perinatal transformation of myocardial metabolism.
authors.affiliation: Center for Pharmacogenomics, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, United States. Electronic address: gdorn@dom.wustl.edu.
authors.forename: Gerald W
authors.initials: GW
authors.lastname: Dorn
mesh_terms: D000818:Animals; D004734:Energy Metabolism; D005786:Gene Expression Regulation; D006321:Heart / Q000502:physiology*; D006801:Humans; D008929:Mitochondria, Heart / Q000378:metabolism*; D063154:Mitochondrial Dynamics; D063306:Mitophagy; D023421:Models, Animal; D009206:Myocardium / Q000378:metabolism*; D044767:Ubiquitin-Protein Ligases / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*
chemical_list: D044767:Ubiquitin-Protein Ligases; C111567:parkin protein