SIRT1 but not its increased expression is essential for lifespan extension in caloric‐restricted mice

Aging Cell

Evi M. Mercken¹  Jia Hu⁴  Susan Krzysik-Walker²  Min Wei⁴  Ying Li⁴  Michael W. McBurney³  Rafael de Cabo¹ 

[1] Translational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA;Laboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA;Department of Medicine, Ottawa Hospital Research Institute, University of Ottawa, Ottawa, Ontario, Canada;Davis School of Gerontology and Department of Biological Sciences, University of Southern California, Los Angeles, CA, USA

关键词: anti‐aging;    caloric restriction;    lifespan;    SIRT1;   

DOI  :  10.1111/acel.12151

来源: Wiley

【 摘 要 】

Summary

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.

【 授权许可】

CC BY   
© 2013 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.

Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.