2024-03-29T12:42:04Zhttp://repisalud.isciii.es/oai/requestoai:repisalud.isciii.es:20.500.12105/52372023-10-13T10:35:55Zcom_20.500.12105_2145com_20.500.12105_2051com_20.500.12105_2144col_20.500.12105_2146
Repisalud
author
Scialo, Filippo
author
Sriram, Ashwin
author
Fernandez-Ayala, Daniel
author
Gubina, Nina
author
Lohmus, Madis
author
Nelson, Glyn
author
Logan, Angela
author
Cooper, Helen M.
author
Navas, Placido
author
Enriquez, Jose Antonio
author
Murphy, Michael P.
author
Sanz, Alberto
funder
Unión Europea. Comisión Europea. European Research Council (ERC)
funder
Finlands Akademi (Finlandia)
funder
Biotechnology and Biological Sciences Research Council (Reino Unido)
funder
Centre for International Mobility (Finlandia)
funder
Medical Research Council (Reino Unido)
funder
Ministerio de Economía y Competitividad (España)
funder
Instituto de Salud Carlos III
2017-10-30T13:32:25Z
2017-10-30T13:32:25Z
2016
Cell Metab. 2016; 23(4):725-34
1550-4131
http://hdl.handle.net/20.500.12105/5237
27076081
10.1016/j.cmet.2016.03.009
1932-7420
Cell Metabolism
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.
eng
INCREASING OXIDATIVE STRESS
CAENORHABDITIS-ELEGANS
DIETARY RESTRICTION
C. ELEGANS
EXPRESSION
LONGEVITY
CATALASE
MITOHORMESIS
RESPIRATION
INHIBITION
Mitochondrial ROS Produced via Reverse Electron Transport Extend Animal Lifespan
journal article
URL
https://repisalud.isciii.es/bitstream/20.500.12105/5237/1/MitochondrialROSProducedVia_2016
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MitochondrialROSProducedVia_2016
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https://repisalud.isciii.es/bitstream/20.500.12105/5237/2/MitochondrialROSProducedVia_2016_suppl1
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MitochondrialROSProducedVia_2016_suppl1
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https://repisalud.isciii.es/bitstream/20.500.12105/5237/3/MitochondrialROSProducedVia_2016_suppl2
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MitochondrialROSProducedVia_2016_suppl2
URL
https://repisalud.isciii.es/bitstream/20.500.12105/5237/20/MitochondrialROSProducedVia_2016.txt
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MitochondrialROSProducedVia_2016.txt
URL
https://repisalud.isciii.es/bitstream/20.500.12105/5237/22/MitochondrialROSProducedVia_2016_suppl1.txt
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MitochondrialROSProducedVia_2016_suppl1.txt