Takagi Hiromitsu, Matsui Yutaka, Sadoshima Junichi
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.
Antioxid Redox Signal. 2007 Sep;9(9):1373-81. doi: 10.1089/ars.2007.1689.
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.
自噬是降解长寿胞质蛋白的主要机制，也是已知唯一的细胞器降解途径。自噬可被多种形式的应激激活，包括营养和能量饥饿、氧化应激、线粒体功能障碍、内质网应激及感染。尽管自噬可回收氨基酸和脂肪酸以产生能量并清除受损细胞器，从而在细胞存活中发挥重要作用，但自噬的不适当激活会导致细胞死亡。在心脏中，可观察到自噬在营养饥饿、缺血/再灌注及心力衰竭时被激活。在本综述中，将讨论心肌缺血和再灌注期间自噬的信号传导机制及其功能意义。
