Does Damage to DNA and Other Macromolecules Play a Role in Aging? If So, How?

被引：80

作者：

Campisi, Judith ^{[1
,2
]}

Vijg, Jan ^{[3
]}

机构：

[1] Univ Calif Berkeley, Lawrence Berkeley Lab, Div Life Sci, Berkeley, CA 94720 USA

[2] Buck Inst Age Res, Novato, CA USA

[3] Albert Einstein Coll Med, Dept Genet, Bronx, NY 10467 USA

来源：

JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES | 2009年 / 64卷 / 02期

关键词：

Apoptosis; Cellular senescence; Reactive oxygen species; LIFE-SPAN; DELETION MUTATIONS; OXIDATIVE DAMAGE; MUSCLE-FIBERS; CAUSAL ROLE; MITOCHONDRIA; MICE; PHENOTYPES; LONGEVITY; CATALASE;

D O I：

10.1093/gerona/gln065

中图分类号：

R592 [老年病学]; C [社会科学总论];

学科分类号：

03 ; 0303 ; 100203 ;

摘要：

One of the most pervasive ideas regarding the causes of aging is that longevity is constrained in large measure by damage to macromolecules. An increasing body of cellular and molecular data, generated over the past decade or so, has generally supported this "damage accumulation" hypothesis of aging. There remain unanswered questions regarding which types of damage are most important for driving aging. In addition, there have been recent challenges to the damage accumulation hypothesis and a new emphasis on the importance of cellular responses and the sequelae to damage, rather damage per se. New tools and approaches are on the horizon and will need to be developed and implemented before we can fully understand whether and to what extent macromolecular damage drives aging phenotypes.

引用

页码：175 / 178

页数：4

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