期刊
CELL METABOLISM
卷 23, 期 4, 页码 725-734出版社
CELL PRESS
DOI: 10.1016/j.cmet.2016.03.009
关键词
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资金
- European Research Council
- Academy of Finland
- BBSRC
- Centre for International Mobility
- Medical Research Council
- Spanish Ministry of Health
- Instituto de Salud Carlos III [FIS PI14-01962]
- Biotechnology and Biological Sciences Research Council [BB/M023311/1] Funding Source: researchfish
- Medical Research Council [MC_U105663142] Funding Source: researchfish
- BBSRC [BB/M023311/1] Funding Source: UKRI
- MRC [MC_U105663142] Funding Source: UKRI
Increased production of reactive oxygen species (ROS) has long been considered a cause of aging. However, recent studies have implicated ROS as essential secondary messengers. Here we show that the site of ROS production significantly contributes to their apparent dual nature. We report that ROS increase with age as mitochondrial function deteriorates. However, we also demonstrate that increasing ROS production specifically through respiratory complex I reverse electron transport extends Drosophila lifespan. Reverse electron transport rescued pathogenesis induced by severe oxidative stress, highlighting the importance of the site of ROS production in signaling. Furthermore, preventing ubiquinone reduction, through knockdown of PINK1, shortens lifespan and accelerates aging; phenotypes that are rescued by increasing reverse electron transport. These results illustrate that the source of a ROS signal is vital in determining its effects on cellular physiology and establish that manipulation of ubiquinone redox state is a valid strategy to delay aging.
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