SIRT6 in DNA repair, metabolism and ageing

被引：124

作者：

Lombard, D. B. ^{[1
,2
,3
]}

Schwer, B. ^{[1
,2
]}

Alt, F. W. ^{[1
,2
]}

Mostoslavsky, R. ^{[1
,2
]}

机构：

[1] Harvard Univ, Sch Med, Howard Hughes Med Inst, Childrens Hosp,CBR Inst Biomed Res, Boston, MA 02115 USA

[2] Harvard Univ, Sch Med, Dept Genet, Boston, MA USA

[3] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA

来源：

JOURNAL OF INTERNAL MEDICINE | 2008年 / 263卷 / 02期

关键词：

ageing; DNA damage; metabolism;

D O I：

10.1111/j.1365-2796.2007.01902.x

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Ageing, or increased mortality with time, coupled with physiologic decline, is a nearly universal yet poorly understood biological phenomenon. Studies in model organisms suggest that two conserved pathways modulate longevity: DNA damage repair and Insulin/Igf1-like signalling. In addition, homologs of yeast Sir2 - the sirtuins - regulate lifespan in diverse organisms. Here, we focus on one particular sirtuin, SIRT6. Mice lacking SIRT6 develop a degenerative disorder that in some respects mimics models of accelerated ageing [Cell (2006) 124:315]. We discuss how sirtuins in general and SIRT6 specifically relate to other evolutionarily conserved pathways affecting ageing, and how SIRT6 might function to ensure organismal homeostasis and normal lifespan.

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页码：128 / 141

页数：14

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