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.
journal_name
Celljournal_title
Cellauthors
Mouchiroud L,Houtkooper RH,Moullan N,Katsyuba E,Ryu D,Cantó C,Mottis A,Jo YS,Viswanathan M,Schoonjans K,Guarente L,Auwerx Jdoi
10.1016/j.cell.2013.06.016subject
Has Abstractpub_date
2013-07-18 00:00:00pages
430-41issue
2eissn
0092-8674issn
1097-4172pii
S0092-8674(13)00755-1journal_volume
154pub_type
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