Journal
AUTOPHAGY
Volume 17, Issue 2, Pages 590-592Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2020.1860490
Keywords
ADH5; ATM; DNA damage; GSNOR; hydrogen peroxide; mitophagy; nitric oxide; oxidative stress; S-nitrosylation; T cell
Categories
Funding
- Novo Nordisk Foundation [2018-0052550]
- Danish Cancer Society [KBVU R146-A9414, R231-A13855]
- Italian Association for Cancer Research [IG2017-20719]
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Mitophagy is a selective process that removes damaged mitochondria and prevents overproduction of ROS, serving as an antioxidant process. ATM is a neglected antioxidant with a role in mitigating chronic oxidative stress through mechanisms like ADH5/GSNOR and PARK2 denitrosylation.
Mitophagy is a selective process aimed at removing damaged or burned-out mitochondria; it is activated upon different stimuli and plays a fundamental role in preventing overproduction of reactive oxygen species (ROS) that might be generated by dysfunctional mitochondria. From this angle, mitophagy can be considered a fully-fledged antioxidant process. Such a surrogate antioxidant function is recently emerging, being shared among many molecular pathways and players that are usually not included among - and, formally, do not directly act as - antioxidants. ATM (ataxia telangiectasia mutated) is a prototype of this class of neglected antioxidants. In spite of its well-known role in DNA damage response, many phenotypes of ataxia telangiectasia (A-T) patients are, indeed, related to chronic oxidative stress, arguing for an additional antioxidant role of ATM. In a recent study, we discovered the mechanism through which ATM exerts antioxidant activity. In particular, we provided evidence that this involves ADH5/GSNOR (alcohol dehydrogenase 5 (class III), chi polypeptide), which, in turn, sustains mitophagy via PARK2 denitrosylation, and protects the cell from detrimental effects due to ROS.
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