ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2021
PTENα is responsible for protection of brain against oxidative stress during aging.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Retinoic Acid Receptor Is a Novel Therapeutic Target for Postoperative Cognitive Dysfunction.Pharmaceutics · 2023Article
- Aging-Associated Thyroid Dysfunction Contributes to Oxidative Stress and Worsened Functional Outcomes Following Traumatic Brain Injury.Antioxidants (Basel, Switzerland) · 2023Article
- Study of molecular patterns associated with ferroptosis in Parkinson's disease and its immune signature.PloS one · 2023Article
- Mesenchymal stem cells and exosomes improve cognitive function in the aging brain by promoting neurogenesis.Frontiers in aging neuroscience · 2022Review
- PTENα is responsible for protection of brain against oxidative stress during aging.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neural cells are continuously subjected to oxidative stress arising from electrochemical activity, and cellular protection systems can turn on the oxidative stress response to detect and alleviate adverse conditions. However, the function and mechanism of the protective systems are complicated and remain largely elusive. We report that PTENα, an isoform of the PTEN family, mediates defense signaling in response to oxidative stress during brain aging. We show that genetic ablation of Ptenα in mice increases oxidative stress and results in neuronal cell death, culminating in accelerated decline of cognition and motor coordination as age increases. PTENα maintains COX activity and promotes energy metabolism through abrogating NEDD4L-mediated degradation of COX4 in response to oxidative stress. In the presence of Parkinson's disease-associated mutation, PTENα loses the capability to protect COX4 and ameliorate defects caused by Ptenα deletion. Our study reveals an important role of PTENα in response to oxidative stress. We propose that dysregulation of PTENα signaling may accelerate the rate of brain aging and promote the development of neurodegenerative disorders.
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Registered trials
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