Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 111, Issue 42, Pages E4458-E4467Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1411199111
Keywords
aging; mitochondria; immunity; reactive oxygen species; C. elegans
Categories
Funding
- National Institutes of Health (NIH)
- National Research Foundation of Korea (NRF) - Korean Government Ministry of Science, Information and Communication Technology, and Future Planning [NRF-2012R1A4A1028200, NRF-2013R1A1A2014754]
- Korean Health Technology Research and Development Project, Ministry of Health and Welfare [HI11C1609]
- NRF [2013M3A9B6076414, 2013018606]
- Ellison Medical Foundation
- NIH/National Institute on Aging [1R01AG044346]
- NRF Grant (Fostering Core Leaders of the Future Basic Science Program) [NRF-2011-0012222]
- National Research Foundation of Korea [2013M3A9B6076414] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Mild inhibition of mitochondrial respiration extends the lifespan of many species. In Caenorhabditis elegans, reactive oxygen species (ROS) promote longevity by activating hypoxia-inducible factor 1 (HIF-1) in response to reduced mitochondrial respiration. However, the physiological role and mechanism of ROS-induced longevity are poorly understood. Here, we show that a modest increase in ROS increases the immunity and lifespan of C. elegans through feedback regulation by HIF-1 and AMP-activated protein kinase (AMPK). We found that activation of AMPK as well as HIF-1 mediates the longevity response to ROS. We further showed that AMPK reduces internal levels of ROS, whereas HIF-1 amplifies the levels of internal ROS under conditions that increase ROS. Moreover, mitochondrial ROS increase resistance to various pathogenic bacteria, suggesting a possible association between immunity and long lifespan. Thus, AMPK and HIF-1 may control immunity and longevity tightly by acting as feedback regulators of ROS.
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