Feedback regulation via AMPK and HIF-1 mediates ROS-dependent longevity in Caenorhabditis elegans
- Feedback regulation via AMPK and HIF-1 mediates ROS-dependent longevity in Caenorhabditis elegans
- Ara B. Hwang; Eun-A Ryu; Murat Artan; Hsin-Wen Chang; Kabir Mohammad Humayun; 남현준; 이동엽; 양재승; 김상욱; William B Mair; 이철주; Siu Sylvia Lee; 이승재
- aging; mitochondria; immunity; reactive oxygen species; C. elegans
- Issue Date
- Proceedings of the National Academy of Sciences of the United States of America
- VOL 111, NO 42, E4458-E4467
- 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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