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• W2012043504 abstract "NAD(+) is an important cofactor regulating metabolic homeostasis and a rate-limiting substrate for sirtuin deacylases. We show that NAD(+) levels are reduced in aged mice and Caenorhabditis elegans and that decreasing NAD(+) levels results in a further reduction in worm lifespan. Conversely, genetic or pharmacological restoration of NAD(+) prevents age-associated metabolic decline and promotes longevity in worms. These effects are dependent upon the protein deacetylase sir-2.1 and involve the induction of mitonuclear protein imbalance as well as activation of stress signaling via the mitochondrial unfolded protein response (UPR(mt)) and the nuclear translocation and activation of FOXO transcription factor DAF-16. Our data suggest that augmenting mitochondrial stress signaling through the modulation of NAD(+) levels may be a target to improve mitochondrial function and prevent or treat age-associated decline." @default.
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• W2012043504 date "2013-07-01" @default.
• W2012043504 modified "2023-10-16" @default.
• W2012043504 title "The NAD+/Sirtuin Pathway Modulates Longevity through Activation of Mitochondrial UPR and FOXO Signaling" @default.
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• W2012043504 doi "https://doi.org/10.1016/j.cell.2013.06.016" @default.
• W2012043504 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3753670" @default.
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