The role of autophagy in mediating cell survival and death during ischemia and reperfusion in the heart.
Autophagy is a major mechanism for degrading long-lived cytosolic proteins and the only known pathway for degrading organelles. Autophagy is activated by many forms of stress, including nutrient and energy starvation, oxidative stress, mitochondrial dysfunction, endoplasmic reticulum stress, and infections. Although autophagy recycles amino acids and fatty acids to produce energy and removes damaged organelles, thereby playing an essential role in cell survival, inappropriate activation of autophagy leads to cell death. In the heart, activation of autophagy can be observed in response to nutrient starvation, ischemia/reperfusion, and heart failure. In this review, the signaling mechanism and the functional significance of autophagy during myocardial ischemia and reperfusion are discussed.
Takagi
Hiromitsu
H
Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark, New Jersey 07103, USA.
Matsui
Yutaka
Y
Sadoshima
Junichi
J
D000818:Animals; D001343:Autophagy; D016923:Cell Death / Q000502:physiology*; D002470:Cell Survival / Q000502:physiology*; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D008322:Mammals; D008954:Models, Biological; D017202:Myocardial Ischemia / Q000473:pathology / Q000503:physiopathology*; D018384:Oxidative Stress; D015424:Reperfusion