Uncoupling protein-2 regulates lifespan in mice

Zane Bruce Andrews, Tamas L Horvath

Research output: Contribution to journalArticleResearchpeer-review

93 Citations (Scopus)


The long-term effects of uncoupled mitochondrial respiration by uncoupling protein 2 (UCP2) in mammalian physiology remains controversial. Here we show that increased mitochondrial uncoupling activity of different tissues predicts longer lifespan of rats compared to 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 life span 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. Key words: mitochondria, ros, mice, aging, sod2.
Original languageEnglish
Pages (from-to)E621 - E627
Number of pages7
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Issue number4
Publication statusPublished - 2009

Cite this