@article{96c459382be743158353332211e2cc15,
title = "Caloric restriction and resveratrol promote longevity through the Sirtuin-1-dependent induction of autophagy",
abstract = "Caloric restriction and autophagy-inducing pharmacological agents can prolong lifespan in model organisms including mice, flies, and nematodes. In this study, we show that transgenic expression of Sirtuin-1 induces autophagy in human cells in vitro and in Caenorhabditis elegans in vivo. The knockdown or knockout of Sirtuin-1 prevented the induction of autophagy by resveratrol and by nutrient deprivation in human cells as well as by dietary restriction in C. elegans. Conversely, Sirtuin-1 was not required for the induction of autophagy by rapamycin or p53 inhibition, neither in human cells nor in C. elegans. The knockdown or pharmacological inhibition of Sirtuin-1 enhanced the vulnerability of human cells to metabolic stress, unless they were stimulated to undergo autophagy by treatment with rapamycin or p53 inhibition. Along similar lines, resveratrol and dietary restriction only prolonged the lifespan of autophagy-proficient nematodes, whereas these beneficial effects on longevity were abolished by the knockdown of the essential autophagic modulator Beclin-1. We conclude that autophagy is universally required for the lifespan-prolonging effects of caloric restriction and pharmacological Sirtuin-1 activators.",
keywords = "ATG7, Caenorhabditis elegans, HCT 116, mTOR, rapamycin, senescence",
author = "E. Morselli and Maiuri, {M. C.} and M. Markaki and E. Megalou and A. Pasparaki and K. Palikaras and A. Criollo and L. Galluzzi and Malik, {S. A.} and I. Vitale and M. Michaud and F. Madeo and N. Tavernarakis and G. Kroemer",
note = "Funding Information: Acknowledgements. We thank Dr Andrew Fire for plasmids. Some nematode strains used in this study were provided by the C. elegans Gene Knockout Project at OMRF (http://www.mutantfactory.ouhsc.edu/), which is part of the International C. elegans Gene Knockout Consortium, and the Caenorhabditis Genetics Center, which was funded by the NIH National Center for Research Resources (NCRR). We thank A Jalil and D Metivier for expert assistance. NT was supported by grants from EMBO, the European Research Council (ERC), and the European Commission Coordination Action ENINET (contract number LSHM-CT-2005-19063). GK was supported by the Ligue Nationale contre le Cancer (Equipe labellis{\'e}e), Agence Nationale pour la Recherche (ANR), European Commission (Apo-Sys, ChemoRes, ApopTrain, Active p53), Fondation pour la Recherche M{\'e}dicale (FRM), Institut National du Cancer (INCa), and Canc{\'e}rop{\^o}le Ile-de-France. EM was funded by a PhD student grant from ApopTrain. LG was supported by the Apo-Sys consortium of the European Union. SAM received a grant from the Higher Education Commission (HEC) of Pakistan.",
year = "2010",
month = jan,
day = "1",
doi = "10.1038/cddis.2009.8",
language = "English",
volume = "1",
journal = "Cell Death and Disease",
issn = "2041-4889",
number = "1",
}