title: Autophagy in the heart:  too much of a good thing?
abstract: Autophagy constitutes a catabolic process involving lysosomal degradation of damaged and redundant cytosolic components into biomolecules, via an elaborate lysosomal pathway. Autophagy is a highly regulated and evolutionary conserved process crucial for normal tissue homeostasis and cell life. Certain members of the Bcl-2 gene family, including the BH3 only protein Bnip3 regulate autophagy during cardiac stress during ischemic or hypoxic injury as means of discarding damaged mitochondria and organelles to avert cell death. Defects in the regulation of autophagy have been associated with a number of human pathologies including cancer, neurodegenerative diseases, and heart failure. Here, we discuss the molecular regulation of autophagy in the heart and cellular demise from "too much a good thing."
authors.affiliation: Departments of Physiology and Pharmacology and Therapeutics, Institute of Cardiovascular Sciences, St Boniface General Hospital Research Center, Room 3016, 351 Taché Avenue, Winnipeg, Manitoba, Canada R2H 2A6.
authors.forename: Erika Y
authors.initials: EY
authors.lastname: Wang
authors.forename: Agnieszka K
authors.initials: AK
authors.lastname: Biala
authors.forename: Joseph W
authors.initials: JW
authors.lastname: Gordon
authors.forename: Lorrie A
authors.initials: LA
authors.lastname: Kirshenbaum
mesh_terms: D000818:Animals; D017209:Apoptosis; D001343:Autophagy; D006333:Heart Failure / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D008247:Lysosomes / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D015398:Signal Transduction; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53