Mitochondrial complex I deactivation is related to superoxide production in acute hypoxia

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dc.contributor.authorHernansanz-Agustín, Pablo
dc.contributor.authorRamos, Elena
dc.contributor.authorNavarro, Elisa
dc.contributor.authorParada, Esther
dc.contributor.authorSánchez-López, Nuria
dc.contributor.authorPeláez-Aguado, Laura
dc.contributor.authorCabrera-García, J. Daniel
dc.contributor.authorTello, Daniel
dc.contributor.authorBuendia, Izaskun
dc.contributor.authorMarina, Anabel
dc.contributor.authorEgea, Javier
dc.contributor.authorLópez, Manuela G.
dc.contributor.authorBogdanova, Anna
dc.contributor.authorMartínez Ruiz, Antonio
dc.date.accessioned2024-04-11T12:26:58Z
dc.date.available2024-04-11T12:26:58Z
dc.date.issued2017-08
dc.description.abstractMitochondria use oxygen as the final acceptor of the respiratory chain, but its incomplete reduction can also produce reactive oxygen species (ROS), especially superoxide. Acute hypoxia produces a superoxide burst in different cell types, but the triggering mechanism is still unknown. Herein, we show that complex I is involved in this superoxide burst under acute hypoxia in endothelial cells. We have also studied the possible mechanisms by which complex I could be involved in this burst, discarding reverse electron transport in complex I and the implication of PTEN-induced putative kinase 1 (PINK1). We show that complex I transition from the active to ‘deactive’ form is enhanced by acute hypoxia in endothelial cells and brain tissue, and we suggest that it can trigger ROS production through its Na+/H+ antiporter activity. These results highlight the role of complex I as a key actor in redox signalling in acute hypoxia.
dc.description.departmentDepto. de Bioquímica y Biología Molecular
dc.description.facultyFac. de Farmacia
dc.description.refereedTRUE
dc.description.sponsorshipSpanish Government
dc.description.sponsorshipFundación Domingo Martínez
dc.description.sponsorshipEuropean Union FEDER/ERDF
dc.description.sponsorshipSwiss National Science Foundation
dc.description.sponsorshipInstituto de Investigación Sanitaria Princesa
dc.description.sponsorshipUniversidad Autónoma de Madrid
dc.description.statuspub
dc.identifier.doi10.1016/j.redox.2017.04.025
dc.identifier.issn2213-2317
dc.identifier.urihttps://hdl.handle.net/20.500.14352/103011
dc.journal.titleRedox Biology
dc.language.isoeng
dc.page.final1051
dc.page.initial1040
dc.relation.projectIDCSD2007- 00020
dc.relation.projectIDinfo:eu-repo/grantAgreement/MINECO//SAF2015-71521-REDC/ES/CONSOLIDACION RED MULTIDISCIPLINAR EN BIOLOGIA REDOX/
dc.relation.projectIDPI12/00875
dc.relation.projectIDinfo:eu-repo/grantAgreement/MINECO//PI15%2F00107/ES/Señalización en hipoxia por especies reactivas de oxígeno, y proteómica redox: de los mecanismos moleculares a las aplicaciones clínicas/
dc.relation.projectIDSAF2013-32223
dc.relation.projectIDinfo:eu-repo/grantAgreement/ME//AP2010-1219/ES/AP2010-1219/
dc.relation.projectIDinfo:eu-repo/grantAgreement/ME//AP2010-1219/ES/AP2010-1219/
dc.relation.projectIDinfo:eu-repo/grantAgreement/MECD//AP2012-5621/ES/AP2012-5621/
dc.relation.projectIDFPI-UAM2012
dc.relation.projectIDCES12/005
dc.relation.projectIDinfo:eu-repo/grantAgreement/MINECO//CP14%2F00008/ES/CP14%2F00008/
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internationalen
dc.rights.accessRightsopen access
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subject.cdu577.1
dc.subject.keywordHypoxia
dc.subject.keywordMitochondrial complex I
dc.subject.keywordRedox signalling
dc.subject.keywordOxygen sensing
dc.subject.keywordSuperoxide
dc.subject.ucmBioquímica (Farmacia)
dc.subject.unesco2302 Bioquímica
dc.titleMitochondrial complex I deactivation is related to superoxide production in acute hypoxia
dc.typejournal article
dc.type.hasVersionAM
dc.volume.number12
dspace.entity.typePublication
relation.isAuthorOfPublicationeec0b303-34c9-47dd-9ec6-704b6c6c7acd
relation.isAuthorOfPublication.latestForDiscoveryeec0b303-34c9-47dd-9ec6-704b6c6c7acd
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