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NAD+ supplementation prevents STING-induced senescence in ataxia telangiectasia by improving mitophagy

Aging Cell

March 18, 2021

Yang, Beimeng

Summary

Senescence phenotypes and mitochondrial dysfunction are implicated in aging and in premature aging diseases, including ataxia telangiectasia (A-T). Loss of mitochondrial function can drive age-related decline in the brain, but little is known about whether improving mitochondrial homeostasis alleviates senescence phenotypes. We demonstrate here that mitochondrial dysfunction and cellular senescence with a senescence-associated secretory phenotype (SASP) occur in A-T patient fibroblasts, and in ATM-deficient cells and mice. Senescence is mediated by stimulator of interferon genes (STING) and involves ectopic cytoplasmic DNA. We further show that boosting intracellular NAD+ levels with nicotinamide riboside (NR) prevents senescence and SASP by promoting mitophagy in a PINK1-dependent manner. NR treatment also prevents neurodegeneration, suppresses senescence and neuroinflammation, and improves motor function in Atm−/− mice. Our findings suggest a central role for mitochondrial dysfunction-induced senescence in A-T pathogenesis, and that enhancing mitophagy as a potential therapeutic intervention.

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I am Shelly Albaum, and this is my personal website and blog. All the opinions presented here are my own. Nobody writes here but me. You can read more about me here. Cookies are not required to use this website. Read more about that here. 

Original work © 2022 by Right of Assembly

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1. Health Supplements Are Not Medicines. Health Supplements that raise NAD levels, like nicotinamide riboside or other NAD precursors, are not intended to diagnose, treat, cure, or prevent any disease.

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