DNA修复、基因组稳定性与衰老。

DNA repair, genome stability, and aging.

作者信息

Lombard David B, Chua Katrin F, Mostoslavsky Raul, Franco Sonia, Gostissa Monica, Alt Frederick W

机构信息

Howard Hughes Medical Institute, The Children's Hospital, Department of Genetics, Harvard Medical School and, The CBR Institute for Biomedical Research, Boston, Massachusetts 02115, USA.

出版信息

Cell. 2005 Feb 25;120(4):497-512. doi: 10.1016/j.cell.2005.01.028.

DOI:10.1016/j.cell.2005.01.028

PMID:15734682

Abstract

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.

摘要

衰老可被定义为随着时间推移而出现的渐进性功能衰退和死亡率上升。在此，我们综述将衰老与核DNA损伤联系起来的证据：DNA损伤随年龄积累，DNA修复缺陷可导致类似早衰的表型。我们讨论细胞DNA损伤反应如何可能导致衰老的表现。我们综述Sir2，这是一个将基因组稳定性、代谢和衰老联系起来的因子。我们最后对突变小鼠在衰老研究中的作用以及未来研究方向进行了一般性讨论。