Standard

The NAD(+)/Sirtuin Pathway Modulates Longevity through Activation of Mitochondrial UPR and FOXO Signaling. / Mouchiroud, Laurent; Houtkooper, Riekelt H.; Moullan, Norman et al.

In: Cell, Vol. 154, No. 2, 2013, p. 430-441.

Research output: Contribution to journalArticleAcademicpeer-review

Harvard

Mouchiroud, L, Houtkooper, RH, Moullan, N, Katsyuba, E, Ryu, D, Cantó, C, Mottis, A, Jo, Y-S, Viswanathan, M, Schoonjans, K, Guarente, L & Auwerx, J 2013, 'The NAD(+)/Sirtuin Pathway Modulates Longevity through Activation of Mitochondrial UPR and FOXO Signaling', Cell, vol. 154, no. 2, pp. 430-441. https://doi.org/10.1016/j.cell.2013.06.016

APA

Mouchiroud, L., Houtkooper, R. H., Moullan, N., Katsyuba, E., Ryu, D., Cantó, C., Mottis, A., Jo, Y-S., Viswanathan, M., Schoonjans, K., Guarente, L., & Auwerx, J. (2013). The NAD(+)/Sirtuin Pathway Modulates Longevity through Activation of Mitochondrial UPR and FOXO Signaling. Cell, 154(2), 430-441. https://doi.org/10.1016/j.cell.2013.06.016

Vancouver

Mouchiroud L, Houtkooper RH, Moullan N, Katsyuba E, Ryu D, Cantó C et al. The NAD(+)/Sirtuin Pathway Modulates Longevity through Activation of Mitochondrial UPR and FOXO Signaling. Cell. 2013;154(2):430-441. doi: 10.1016/j.cell.2013.06.016

Author

Mouchiroud, Laurent ; Houtkooper, Riekelt H. ; Moullan, Norman et al. / The NAD(+)/Sirtuin Pathway Modulates Longevity through Activation of Mitochondrial UPR and FOXO Signaling. In: Cell. 2013 ; Vol. 154, No. 2. pp. 430-441.

BibTeX

@article{1fcc2dfbacc9428da1d21b6e28982dfd,
title = "The NAD(+)/Sirtuin Pathway Modulates Longevity through Activation of Mitochondrial UPR and FOXO Signaling",
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",
author = "Laurent Mouchiroud and Houtkooper, {Riekelt H.} and Norman Moullan and Elena Katsyuba and Dongryeol Ryu and Carles Cant{\'o} and Adrienne Mottis and Young-Suk Jo and Mohan Viswanathan and Kristina Schoonjans and Leonard Guarente and Johan Auwerx",
year = "2013",
doi = "10.1016/j.cell.2013.06.016",
language = "English",
volume = "154",
pages = "430--441",
journal = "Cell",
issn = "0092-8674",
publisher = "Cell Press",
number = "2",

}

RIS

TY - JOUR

T1 - The NAD(+)/Sirtuin Pathway Modulates Longevity through Activation of Mitochondrial UPR and FOXO Signaling

AU - Mouchiroud, Laurent

AU - Houtkooper, Riekelt H.

AU - Moullan, Norman

AU - Katsyuba, Elena

AU - Ryu, Dongryeol

AU - Cantó, Carles

AU - Mottis, Adrienne

AU - Jo, Young-Suk

AU - Viswanathan, Mohan

AU - Schoonjans, Kristina

AU - Guarente, Leonard

AU - Auwerx, Johan

PY - 2013

Y1 - 2013

N2 - 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

AB - 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

U2 - 10.1016/j.cell.2013.06.016

DO - 10.1016/j.cell.2013.06.016

M3 - Article

C2 - 23870130

VL - 154

SP - 430

EP - 441

JO - Cell

JF - Cell

SN - 0092-8674

IS - 2

ER -

ID: 2194074