Calorie restriction promotes mammalian cell survival by inducing the SIRT1 deacetylase

被引：1575

作者：

Cohen, HY

Miller, C

Bitterman, KJ

Wall, NR

Hekking, B

Kessler, B

Howitz, KT

Gorospe, M

de Cabo, R

Sinclair, DA

机构：

[1] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA

[2] BIOMOL Res Labs, Plymouth Meeting, PA 19462 USA

[3] NIA, Cellular & Mol Biol Lab, Gerontol Res Ctr, Baltimore, MD 21224 USA

[4] NIA, Lab Expt Gerontol, Gerontol Res Ctr, Baltimore, MD 21224 USA

来源：

SCIENCE | 2004年 / 305卷 / 5682期

关键词：

D O I：

10.1126/science.1099196

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

A major cause of aging is thought to result from the cumulative effects of cell loss over time. In yeast, caloric restriction (CR) delays aging by activating the Sir2 deacetylase. Here we show that expression of mammalian Sir2 (SIRT1) is induced in CR rats as well as in human cells that are treated with serum from these animals. Insulin and insulin-like growth factor 1 (IGF-1) attenuated this response. SIRT1 deacetylates the DNA repair factor Ku70, causing it to sequester the proapoptotic factor Bax away from mitochondria, thereby inhibiting stress-induced apoptotic cell death. Thus, CR could extend life-span by inducing SIRT1 expression and promoting the long-term survival of irreplaceable cells.

引用

页码：390 / 392

页数：3

共 24 条

[1] Nicotinamide and PNC1 govern lifespan extension by calorie restriction in Saccharomyces cerevisiae [J].