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Roles of Autophagy in Oxidative Stress. | LitMetric

Roles of Autophagy in Oxidative Stress.

Int J Mol Sci

Biomedical Science Institute, Kyung Hee University, Seoul 02447, Korea.

Published: May 2020

AI Article Synopsis

  • - Autophagy is a process that breaks down unnecessary or damaged components in cells via lysosomes, playing a vital role in various biological processes including cell death, stress response, and organelle maintenance.
  • - It acts as a major sensor for redox signaling, responding to reactive oxygen species (ROS), which can either help or harm cells depending on their levels and location.
  • - Understanding the balance between autophagy and cell death is crucial for grasping how redox signaling contributes to disease mechanisms.

Article Abstract

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.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7246723PMC
http://dx.doi.org/10.3390/ijms21093289DOI Listing

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