Document Type
Article
Version Deposited
Published Version
Publication Date
5-8-2018
Publication Title
Oxidative Medicine & Cellular Longevity
DOI
10.1155/2018/4701275
Abstract
Autophagy is a widely conserved catabolic process that is necessary for maintaining cellular homeostasis under normal physiological conditions and driving the cell to switch back to this status quo under times of starvation, hypoxia, and oxidative stress. The potential similarities and differences between basal autophagy and stimulus-induced autophagy are still largely unknown. Both act by clearing aberrant or unnecessary cytoplasmic material, such as misfolded proteins, supernumerary and defective organelles. The relationship between reactive oxygen species (ROS) and autophagy is complex. Cellular ROS is predominantly derived from mitochondria. Autophagy is triggered by this event, and by clearing the defective organelles effectively, it lowers cellular ROS thereby restoring cellular homeostasis. However, if cellular homeostasis cannot be reached, the cells can switch back and choose a regulated cell death response. Intriguingly, the autophagic and cell death machines both respond to the same stresses and share key regulatory proteins, suggesting that the pathways are intricately connected. Here, the intersection between autophagy and apoptosis is discussed with a particular focus on the role ROS plays.
Recommended Citation
Thevissen, Karin & Cooper, Katrina F. Till Death Do Us Part: The Marriage of Autophagy and Apoptosis. Oxidative Medicine and Cellular Longevity 2018, May 8. https://doi.org/10.1155/2018/4701275
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.
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