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

被引:85
作者
Mercken, Evi M. [1 ]
Hu, Jia [2 ,3 ]
Krzysik-Walker, Susan [4 ]
Wei, Min [2 ,3 ]
Li, Ying [2 ,3 ]
McBurney, Michael W. [5 ]
de Cabo, Rafael [1 ]
Longo, Valter D. [2 ,3 ]
机构
[1] NIA, Translat Gerontol Branch, NIH, Baltimore, MD 21224 USA
[2] Univ So Calif, Davis Sch Gerontol, Los Angeles, CA 90089 USA
[3] Univ So Calif, Dept Biol Sci, Los Angeles, CA 90089 USA
[4] NIA, Lab Clin Invest, NIH, Baltimore, MD 21224 USA
[5] Univ Ottawa, Ottawa Hosp Res Inst, Dept Med, Ottawa, ON K1H 8L6, Canada
关键词
anti-aging; caloric restriction; lifespan; SIRT1; PROTECTS;
D O I
10.1111/acel.12151
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:193 / 196
页数:4
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