Roles of Autophagy in Oxidative Stress

• Published in: International journal of molecular sciences Vol. 21; no. 9; p. 3289
• Main Authors: Yun, Hyeong Rok, Jo, Yong Hwa, Kim, Jieun, Shin, Yoonhwa, Kim, Sung Soo, Choi, Tae Gyu
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 06-05-2020; MDPI
• Subjects: Animals; Apoptosis; Autophagy; Biological activity; Cardiovascular Diseases - metabolism; Cell death; Cellular stress response; Diabetes Mellitus - metabolism; Endoplasmic reticulum; Enzymes; Homeostasis; Humans; Hypoxia; Intracellular signalling; Kinases; Low level; Lysosomes; Mitochondria; Neoplasms - metabolism; Neurodegenerative Diseases - metabolism; Organelles; Oxidative Stress; Pathogenesis; Phagocytosis; Phosphorylation; Physiology; Proteins; reactive oxygen species; Review; Signal transduction; oxidative stress; autophagy; reactive oxygen species
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms21093289

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.