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Am J Physiol Endocrinol Metab 296: E621-E627, 2009. First published January 13, 2009; doi:10.1152/ajpendo.90903.2008
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EDITORIAL FOCUS

Uncoupling protein-2 regulates lifespan in mice

Zane B. Andrews1,2,3 and Tamas L. Horvath1,2,4

1Section of Comparative Medicine and Departments of 2Obstetrics, Gynecology, and Reproductive Sciences and 4Neurobiology, Yale University School of Medicine, New Haven, Connecticut; and 3Department of Physiology, Monash University, Clayton, Victoria, Australia

Submitted 10 November 2008 ; accepted in final form 31 December 2008

ABSTRACT

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.

reactive oxygen species; mitochondria; superoxide dismutase-2; longevity; aging; fatty acid oxidation


Address for reprint requests and other correspondence: T. L. Horvath or Z. B. Andrews, Section of Comparative Medicine and Depts. of Obstretics, Gynecology, and Reproductive Sciences, Yale University School of Medicine, 375 Congress Ave., LSOG 117, New Haven, CT 06519 (e-mail: tamas.horvath{at}yale.edu or zane.andrews{at}med.monash.edu.au)




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