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KMID : 1134220130330020083
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Hanyang Medical Reviews
2013 Volume.33 No. 2 p.83 ~ p.89
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Autophagy in Redox SignallingAutophagy is a major catabolic process that is involved in cellular degradation of unnecessary or dysfunctional cellular components via the lysosomal machinery. Autophagy is involved in a variety of biological processes such as programmed cell death, removal of damaged organelles and development of different tissue-specific functions. In recent experiments, the role of autophagy as an important mediator of the pathological response to redox signalling of cellular damage has been elucidated and expanded. Oxidative stresses to the cellular system induces autophagy as a means to selectively remove oxidatively modified macromolecules and organelles. Reactive oxygen species (ROS) are highly reactive oxygen free radicals that are produced as by-products of cellular metabolism, primarily by mitochondria and NADPH oxidases. ROS can be beneficial or harmful to cells and tissues by depending on their concentration and location. ROS function as redox messengers in intracellular signalling at physiologically low level, whereas excess ROS can induce oxidative modification of cellular macromolecules and eventually promote cell death. Thus, the interface of autophagy-related oxidative stress adaptation and cell death is important for understanding redox biology and pathogenesis. In this review, we describe the basic mechanism and function of autophagy in the context of response to oxidative stress and redox signalling in pathogenesis.
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Choi Tae-Gyu
Kim Sung-Soo
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Abstract
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Autophagy is a major catabolic process that is involved in cellular degradation of unnecessary or dysfunctional cellular components via the lysosomal machinery. Autophagy is involved in a variety of biological processes such as programmed cell death, removal of damaged organelles and development of different tissue-specific functions. In recent experiments, the role of autophagy as an important mediator of the pathological response to redox signalling of cellular damage has been elucidated and expanded. Oxidative stresses to the cellular system induces autophagy as a means to selectively remove oxidatively modified macromolecules and organelles. Reactive oxygen species (ROS) are highly reactive oxygen free radicals that are produced as by-products of cellular metabolism, primarily by mitochondria and NADPH oxidases. ROS can be beneficial or harmful to cells and tissues by depending on their concentration and location. ROS function as redox messengers in intracellular signalling at physiologically low level, whereas excess ROS can induce oxidative modification of cellular macromolecules and eventually promote cell death. Thus, the interface of autophagy-related oxidative stress adaptation and cell death is important for understanding redox biology and pathogenesis. In this review, we describe the basic mechanism and function of autophagy in the context of response to oxidative stress and redox signalling in pathogenesis.
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KEYWORD
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Autophagy, Cell Death, Reactive Oxygen Species, Oxidation-Reduction
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