Sirtuins, Aging, and Metabolism

被引:159
作者
Guarente, Leonard [1 ,2 ]
机构
[1] MIT, Paul F Glenn Lab, 77 Massachusetts Ave, Cambridge, MA 02139 USA
[2] MIT, Dept Biol, Cambridge, MA 02139 USA
来源
METABOLISM AND DISEASE | 2011年 / 76卷
基金
美国国家卫生研究院;
关键词
SMALL-MOLECULE ACTIVATORS; FATTY-ACID OXIDATION; CALORIE RESTRICTION; SIR2; HOMOLOG; LIFE-SPAN; SIRT3-MEDIATED DEACETYLATION; SACCHAROMYCES-CEREVISIAE; CELLULAR-METABOLISM; GENE; ACETYLATION;
D O I
10.1101/sqb.2011.76.010629
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Sirtuins are nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylases that link protein acetylation, metabolism, aging, and diseases of aging. Sirtuins were initially found to slow aging in lower organisms and more recently shown to mediate many effects of calorie restriction on metabolism and longevity in mammals. This chapter focuses on two key mammalian sirtuins, SIRT1 (which resides mainly in the nucleus) and SIRT3 (which is mitochondrial). I discuss the many protein substrates of these sirtuins and how they determine the metabolic strategy most efficacious under scarce or abundant food supplies. I also discuss the logic by which sirtuins link protein acetylation and metabolism. Finally, I discuss emerging data showing protection by sirtuins against most of the common diseases of aging. It is possible that sirtuins will be novel targets to combat these diseases pharmacologically.
引用
收藏
页码:81 / 90
页数:10
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