title: Autophagy: a novel protective mechanism in chronic ischemia.
abstract: During the search for cardioprotective mechanisms in a porcine model of chronic myocardial ischemia and hibernating myocardium, we discovered evidence for autophagy, which could be involved in the protection against apoptosis. Autophagy is a cellular degradation process responsible for the turnover of unnecessary or dysfunctional organelles and cytoplasmic proteins, which become sequestered in a double-membrane-bound vesicle, termed autophagosome, and subsequently degrade upon fusion with lysosomes. The dauer phase in C. elegans shares similarities with the induction of autophagy in chronically ischemic (hibernating) myocardium. In this sense, autophagy is an essential mechanism for survival which is activated by environmental stresses and confers stress resistance to the organism. Our study provided insight into understanding of the protective mechanism of autophagy in chronic ischemia.
authors.affiliation: Department of Cell Biology and Molecular Medicine and Cardiovascular Research Institute, UMDNJ-New Jersey Medical School, Newark, New Jersey, USA.
authors.forename: Lin
authors.initials: L
authors.lastname: Yan
authors.forename: Junichi
authors.initials: J
authors.lastname: Sadoshima
authors.forename: Dorothy E
authors.initials: DE
authors.lastname: Vatner
authors.forename: Stephen F
authors.initials: SF
authors.lastname: Vatner
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D017209:Apoptosis; D001343:Autophagy; D002908:Chronic Disease; D017202:Myocardial Ischemia / Q000473:pathology*; D017682:Myocardial Stunning; D013312:Stress, Physiological