Taking a "good" look at free radicals in the aging process

被引：442

作者：

Hekimi, Siegfried ^{[1
]}

Lapointe, Jerome ^{[1
]}

Wen, Yang ^{[1
]}

机构：

[1] McGill Univ, Dept Biol, Montreal, PQ H3A 1B1, Canada

来源：

TRENDS IN CELL BIOLOGY | 2011年 / 21卷 / 10期

关键词：

MN SUPEROXIDE-DISMUTASE; LONGEST-LIVING RODENT; FIBROSIS-RELATED GENES; ELEGANS LIFE-SPAN; OXIDATIVE DAMAGE; HYDROGEN-PEROXIDE; DNA-DAMAGE; MITOCHONDRIAL DYSFUNCTION; DILATED CARDIOMYOPATHY; COLLAGEN DEPOSITION;

D O I：

10.1016/j.tcb.2011.06.008

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The mitochondrial free radical theory of aging (MFRTA) proposes that aging is caused by damage to macromolecules by mitochondrial reactive oxygen species (ROS). This is based on the observed association of the rate of aging and the aged phenotype with the generation of ROS and oxidative damage. However, recent findings, in particular in Caenorhabditis elegans but also in rodents, suggest that ROS generation is not the primary or initial cause of aging. Here, we propose that ROS are tightly associated with aging because they play a role in mediating a stress response to age-dependent damage. This could generate the observed correlation between aging and ROS without implying that ROS damage is the earliest trigger or main cause of aging.

引用

页码：569 / 576

页数：8

共 88 条

[1] Disparate patterns of age-related changes in lipid peroxidation in long-lived naked mole-rats and shorter-lived mice [J].