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dc.contributor.authorScialo, Filippo
dc.contributor.authorSriram, Ashwin
dc.contributor.authorFernandez-Ayala, Daniel
dc.contributor.authorGubina, Nina
dc.contributor.authorLohmus, Madis
dc.contributor.authorNelson, Glyn
dc.contributor.authorLogan, Angela
dc.contributor.authorCooper, Helen M.
dc.contributor.authorNavas, Placido
dc.contributor.authorEnriquez, Jose Antonio 
dc.contributor.authorMurphy, Michael P.
dc.contributor.authorSanz, Alberto
dc.date.accessioned2017-10-30T13:32:25Z
dc.date.available2017-10-30T13:32:25Z
dc.date.issued2016
dc.identifierISI:000374123200019
dc.identifier.citationCell Metab. 2016; 23(4):725-34
dc.identifier.issn1550-4131
dc.identifier.urihttp://hdl.handle.net/20.500.12105/5237
dc.description.abstractIncreased 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.
dc.description.sponsorshipThis work was supported by the European Research Council (ERC Starting Grant to A. Sanz), the Academy of Finland (Academy Research Fellowship to A. Sanz and Postdoctoral Research grant to H.M.C), the BBSRC (Responsive mode grant to A. Sanz), the Centre for International Mobility (Postdoctoral fellowship to N.G.), the Medical Research Council (M.P.M), and the Spanish Ministry of Health and the Instituto de Salud Carlos III (FIS PI14-01962 to P.N.). Electron microscopy image processing was performed at the Laboratory of Electron Microscopy, University of Turku, Finland. We thank Dr Rhoda Stefanatos for help with editing the manuscript. The authors declare no competing financial interests.
dc.language.isoeng
dc.publisherCell Press 
dc.type.hasVersionVoR
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectINCREASING OXIDATIVE STRESS
dc.subjectCAENORHABDITIS-ELEGANS
dc.subjectDIETARY RESTRICTION
dc.subjectC. ELEGANS
dc.subjectEXPRESSION
dc.subjectLONGEVITY
dc.subjectCATALASE
dc.subjectMITOHORMESIS
dc.subjectRESPIRATION
dc.subjectINHIBITION
dc.titleMitochondrial ROS Produced via Reverse Electron Transport Extend Animal Lifespan
dc.typejournal article
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.identifier.pubmedID27076081
dc.format.volume23
dc.format.page725-734
dc.identifier.doi10.1016/j.cmet.2016.03.009
dc.contributor.funderUnión Europea. Comisión Europea. European Research Council (ERC) 
dc.contributor.funderFinlands Akademi (Finlandia) 
dc.contributor.funderBiotechnology and Biological Sciences Research Council (Reino Unido) 
dc.contributor.funderCentre for International Mobility (Finlandia) 
dc.contributor.funderMedical Research Council (Reino Unido) 
dc.contributor.funderMinisterio de Economía y Competitividad (España) 
dc.contributor.funderInstituto de Salud Carlos III 
dc.description.peerreviewed
dc.identifier.e-issn1932-7420
dc.relation.publisherversionhttps://doi.org/10.1016/j.cmet.2016.03.009
dc.identifier.journalCell Metabolism
dc.repisalud.orgCNICCNIC::Grupos de investigación::Genética Funcional del Sistema de Fosforilación Oxidativa
dc.repisalud.institucionCNIC
dc.rights.accessRightsopen accesses_ES


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Attribution-NonCommercial-NoDerivatives 4.0 Internacional
Este Item está sujeto a una licencia Creative Commons: Attribution-NonCommercial-NoDerivatives 4.0 Internacional