These authors contributed equally to this research.
SIRT1 but not its increased expression is essential for lifespan extension in caloric-restricted mice
Article first published online: 19 NOV 2013
© 2013 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Volume 13, Issue 1, pages 193–196, February 2014
How to Cite
Mercken, E. M., Hu, J., Krzysik-Walker, S., Wei, M., Li, Y., McBurney, M. W., de Cabo, R. and Longo, V. D. (2014), SIRT1 but not its increased expression is essential for lifespan extension in caloric-restricted mice. Aging Cell, 13: 193–196. doi: 10.1111/acel.12151
- Issue published online: 16 JAN 2014
- Article first published online: 19 NOV 2013
- Accepted manuscript online: 14 AUG 2013 05:06AM EST
- Manuscript Accepted: 8 AUG 2013
- NIH/NIA . Grant Numbers: AG20642, AG025135, AG034906
- caloric restriction;
The SIRT1 deacetylase is one of the best-studied putative mediators of some of the anti-aging effects of calorie restriction (CR), but its role in CR-dependent lifespan extension has not been demonstrated. We previously found that mice lacking both copies of SIRT1 displayed a shorter median lifespan than wild-type mice on an ad libitum diet. Here, we report that median lifespan extension in CR heterozygote SIRT1+/− mice was identical (51%) to that observed in wild-type mice, but SIRT1+/− mice displayed a higher frequency of certain pathologies. Although larger studies in additional genetic backgrounds are needed, these results provide strong initial evidence for the requirement of SIRT1 for the lifespan extension effects of CR, but suggest that its high expression is not required for CR-induced lifespan extension.