Roles of Autophagy in Oxidative Stress

被引:359
作者
Yun, Hyeong Rok [1 ,2 ]
Jo, Yong Hwa [2 ,3 ]
Kim, Jieun [2 ,3 ]
Shin, Yoonhwa [1 ,2 ]
Kim, Sung Soo [1 ,2 ,3 ]
Choi, Tae Gyu [2 ,3 ]
机构
[1] Kyung Hee Univ, Grad Sch, Dept Biomed Sci, Seoul 02447, South Korea
[2] Kyung Hee Univ, Biomed Sci Inst, Seoul 02447, South Korea
[3] Kyung Hee Univ, Sch Med, Dept Biochem & Mol Biol, Seoul 02447, South Korea
基金
新加坡国家研究基金会;
关键词
autophagy; reactive oxygen species; oxidative stress; TRANSCRIPTION FACTOR NRF2; CANCER STEM-CELLS; MAMMALIAN AUTOPHAGY; HYDROGEN-PEROXIDE; MOLECULAR-MECHANISMS; MITOCHONDRIAL DYSFUNCTION; TAU PHOSPHORYLATION; SIGNAL-TRANSDUCTION; COMPLEX CONTRIBUTES; SELECTIVE AUTOPHAGY;
D O I
10.3390/ijms21093289
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Autophagy is a catabolic process for unnecessary or dysfunctional cytoplasmic contents by lysosomal degradation pathways. Autophagy is implicated in various biological processes such as programmed cell death, stress responses, elimination of damaged organelles and development. The role of autophagy as a crucial mediator has been clarified and expanded in the pathological response to redox signalling. Autophagy is a major sensor of the redox signalling. Reactive oxygen species (ROS) are highly reactive molecules that are generated as by-products of cellular metabolism, principally by mitochondria. Mitochondrial ROS (mROS) are beneficial or detrimental to cells depending on their concentration and location. mROS function as redox messengers in intracellular signalling at physiologically low level, whereas excessive production of mROS causes oxidative damage to cellular constituents and thus incurs cell death. Hence, the balance of autophagy-related stress adaptation and cell death is important to comprehend redox signalling-related pathogenesis. In this review, we attempt to provide an overview the basic mechanism and function of autophagy in the context of response to oxidative stress and redox signalling in pathology.
引用
收藏
页数:27
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