DNA repair, genome stability, and aging

被引：721
作者：
Lombard, DB
Chua, KF
Mostoslavsky, R
Franco, S
Gostissa, M
Alt, FW [1 ]
机构：
[1] Harvard Univ, Childrens Hosp, Sch Med,Howard Hughes Med Inst, Dept Genet, Boston, MA 02115 USA
[2] CBR Inst Biomed Res, Boston, MA USA
[3] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA
来源：
CELL | 2005年 / 120卷 / 04期
基金：
美国国家卫生研究院;
关键词：
D O I：
10.1016/j.cell.2005.01.028
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：
Aging can be defined as progressive functional decline and increasing mortality over time. Here, we review evidence linking aging to nuclear DNA lesions: DNA damage accumulates with age, and DNA repair defects can cause phenotypes resembling premature aging. We discuss how cellular DNA damage responses may contribute to manifestations of aging. We review Sir2, a factor linking genomic stability, metabolism, and aging. We conclude with a general discussion of the role of mutant mice in aging research and avenues for future investigation.
引用
收藏
页码：497 / 512
页数：16
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