Advances in Sirtuin on The Mechanism of Calorie Restriction on Lifespan

被引:2
|
作者
Liu Bin [1 ,2 ]
Chen Wei-Chun [1 ,3 ]
Liu Xin-Guang [1 ,2 ,3 ]
Zhou Zhong-Jun [4 ]
机构
[1] Guangdong Med Coll, Inst Aging Res, Dongguan 523808, Peoples R China
[2] Key Lab Med Mol Diagnost Guangdong Prov, Dongguan 523808, Peoples R China
[3] Guangdong Med Coll, Inst Biochem & Mol Biol, Zhanjiang 524023, Peoples R China
[4] Univ Hong Kong, Dept Biochem, Li Ka Shing Fac Med, Hong Kong, Hong Kong, Peoples R China
基金
中国国家自然科学基金;
关键词
aging; caloric restriction; lifespan; Sir2; SIRT1; CAENORHABDITIS-ELEGANS; DNA-REPAIR; MITOCHONDRIAL-FUNCTION; LONGEVITY REGULATION; DIETARY RESTRICTION; OXIDATIVE STRESS; CELL-SURVIVAL; SIR2; YEAST; NICOTINAMIDE;
D O I
10.3724/SP.J.1206.2011.00146
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Caloric restriction(CR) can delay aging and the onset of aging-related diseases. Sirtuin plays a key role in the aging process regulated by CR because of its ability to sense the metabolic status and to integrate into adaptive transcriptional outputs. Sirtuin regulates the aging process by altering protein activity and stability through lysine acetylation. Moderate CR in yeast influences replicative lifespan and chronological lifespan mainly by increasing the NAD(+)/NADH ratio and regulating the level of nicotinamide. Similar mechanism also exist among Caenorhabditis elegans and Drosophila melanogasters. SIRT1 protein level increases in response to CR in mammals, leading to an increase in PNC1/Nampt expression, which favors the synthesis of NAD+ from NAM, potentially acting as a major mechanism to drop the leash of SIRT1 inhibition. NO up-regulates SIRT1 and mitochondrial biogenesis. Cellular and organism's senescence may be influenced through the deacetylation of histone, p53, NES1, FOXO by SIRT1, indicating sirtuin and its homologous analogues play important roles in aging process and lifespan extension under CR in different organisms.
引用
收藏
页码:5 / 13
页数:9
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