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- W2791478032 abstract "Significance The free radical theory of aging remains controversial. Accumulation of mitochondrial damage is commonly accepted as an age-related phenomenon associated with the inescapable side effects of oxidative metabolism. However, to date, molecular determinants of this phenomenon have not been identified. Previous evidence indicates that engineered mice deficient in the denitrosylase S -nitrosoglutathione reductase (GSNOR) show features of aging. Here, we show that due to epigenetic events, GSNOR expression declines with age, ultimately resulting in the accumulation of damaged mitochondria. By contrast, centenarians maintain high GSNOR expression. Collectively, these data suggest that GSNOR may act as a longevity protein countering defects in mitochondrial physiology that arise from age-related epigenetic deregulation." @default.
- W2791478032 created "2018-03-29" @default.
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- W2791478032 date "2018-03-26" @default.
- W2791478032 modified "2023-10-16" @default.
- W2791478032 title "<i>S</i> -nitrosylation drives cell senescence and aging in mammals by controlling mitochondrial dynamics and mitophagy" @default.
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- W2791478032 doi "https://doi.org/10.1073/pnas.1722452115" @default.
- W2791478032 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5899480" @default.
- W2791478032 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29581312" @default.
- W2791478032 hasPublicationYear "2018" @default.
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