Uncoupling protein-2 regulates lifespan in mice

被引:85
作者
Andrews, Zane B. [1 ,2 ,3 ]
Horvath, Tamas L. [1 ,2 ,4 ]
机构
[1] Yale Univ, Sch Med, Comparat Med Sect, New Haven, CT 06519 USA
[2] Yale Univ, Sch Med, Dept Obstet Gynecol & Reprod Sci, New Haven, CT 06519 USA
[3] Yale Univ, Sch Med, Dept Neurobiol, New Haven, CT 06519 USA
[4] Monash Univ, Dept Physiol, Clayton, Vic 3168, Australia
来源
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM | 2009年 / 296卷 / 04期
关键词
reactive oxygen species; mitochondria; superoxide dismutase-2; longevity; aging; fatty acid oxidation; PREVENTS NEURONAL DEATH; BETA-CELL DYSFUNCTION; KNOCKOUT MICE; MITOCHONDRIAL; EXPRESSION; GLUCOSE; OBESITY; INJURY; GENE; UCP2;
D O I
10.1152/ajpendo.90903.2008
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Andrews ZB, Horvath TL. Uncoupling protein-2 regulates lifespan in mice. Am J Physiol Endocrinol Metab 296: E621-E627, 2009. First published January 13, 2009; doi:10.1152/ajpendo.90903.2008. The long-term effects of uncoupled mitochondrial respiration by uncoupling protein-2 (UCP2) in mammalian physiology remain controversial. Here we show that increased mitochondrial uncoupling activity of different tissues predicts longer lifespan of rats compared with mice. UCP2 reduces reactive oxygen species (ROS) production and oxidative stress throughout the aging process in different tissues in mice. The absence of UCP2 shortens lifespan in wild-type mice, and the level of UCP2 positively correlates with the postnatal survival of superoxide dismutase-2 mutant animals. Thus UCP2 has a beneficial influence on cell and tissue function leading to increased lifespan.
引用
收藏
页码:E621 / E627
页数:7
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