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Kirshenbaum, Lorrie A. PhD*,†,‡
Departments of *Physiology and
†Pharmacology and Therapeutics
‡The Institute of Cardiovascular Sciences, St Boniface Hospital Research Centre, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
Over the past 2 decades, there has been considerable interest in defining the molecular signaling pathways that govern autophagy in health and disease. Autophagy is an evolutionarily conserved catabolic process that allows recycling of proteins and damaged organelles through a lysosomal-mediated pathway. Autophagy is an essential mechanism for supplying the cell with nutrients for energy production during nutrient stress and removal of damaged organelles during pathogen invasion. Notably, autophagy has been detected in a variety of human cardiomyopathies including ischemic heart disease, Danon disease, myocardial infarction, and heart failure. At present, there is considerable debate as to whether autophagy is an adaptive, maladaptive, or an epiphenomenon associated with the underlying pathology. The ability to modulate autophagy in the heart would be of significant therapeutic value in treating disease entities in which the underlying defect is associated with either inadequate autophagy (accumulation of cytotoxic proteins) or otherwise deregulated autophagy (excessive lysosomal activity) contributes to the underlying pathology. In this focused issue on Autophagy in the Journal of Cardiovascular Pharmacology, several theories and leading views regarding the role of autophagy in heart in health and disease are presented.
This article has been cited 1 time(s).
© 2012 Lippincott Williams & Wilkins, Inc.
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