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dc.creatorCordero, Mario D.es
dc.creatorDíaz-Parrado, Eduardoes
dc.creatorCarrión, Ángel Manueles
dc.creatorAlfonsi, Simonaes
dc.creatorSánchez Alcázar, José Antonioes
dc.creatorMiguel Rodríguez, Manuel de
dc.creatorBattino, Maurizio
dc.creatorMiguel Rodríguez, Manuel de
dc.date.accessioned2019-01-24T17:54:03Z
dc.date.available2019-01-24T17:54:03Z
dc.date.issued2013
dc.identifier.citationBullon, P., Cordero, M.D., Díaz-Parrado, E., Carrión, Á.M., Alfonsi, S. y Sánchez Alcázar, J.A. (2013). Is Inflammation a Mitochondrial Dysfunction-Dependent Event in Fibromyalgia?. Antioxidants and redox signaling, 18 (7), 800-807.
dc.identifier.issn1557-7716es
dc.identifier.urihttps://hdl.handle.net/11441/82046
dc.description.abstractFibromyalgia (FM) is a complex disorder that affects up to 5% of the general population worldwide. Both mitochondrial dysfunction and inflammation have been implicated in the pathophysiology of FM. We have investigated the possible relationship between mitochondrial dysfunction, oxidative stress, and inflammation in FM. We studied 30 women diagnosed with FM and 20 healthy women. Blood mononuclear cells (BMCs) from FM patients showed reduced level of coenzyme Q10 (CoQ10) and mtDNA contents and high level of mitochondrial reactive oxygen species (ROS) and serum tumor necrosis factor (TNF)-alpha and transcript levels. A significant negative correlation between CoQ10 and TNF-alpha levels (r= -0.588; p < 0.01), and a positive correlation between ROS and TNF-alpha levels (r = 0.791; p < 0.001) were observed accompanied by a significant correlation of visual analogical scale with serum TNF-alpha and transcript levels (r = 0.4507; p < 0.05 and r = 0.7089; p < 0.001, respectively). TNF-alpha release was observed in an in vitro (BMCs) and in vivo (mice) CoQ10 deficiency model. Oral CoQ10 supplementation restored biochemical parameters and induced a significant improvement in clinical symptoms ( p < 0.001). These results lead to the hypothesis that inflammation could be a mitochondrial dysfunction-dependent event implicated in the pathophysiology of FM in several patients indicating at mitochondria as a possible new therapeutic target.es
dc.description.sponsorshipUnión Europea FIS PI10/00543es
dc.description.sponsorshipServicio Andaluz de Salud Junta de Andalucía SAS 111242es
dc.description.sponsorshipJunta de Andalucía CTS-5725es
dc.formatapplication/pdfes
dc.language.isoenges
dc.publisherMary Ann Liebert, Inc.es
dc.relation.ispartofAntioxidants and redox signaling, 18 (7), 800-807.
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectFibromyalgiaes
dc.subjectmitochondrial dysfunctiones
dc.subjectinflammationes
dc.subjectFMes
dc.titleIs Inflammation a Mitochondrial Dysfunction-Dependent Event in Fibromyalgia?es
dc.typeinfo:eu-repo/semantics/articlees
dcterms.identifierhttps://ror.org/03yxnpp24
dc.type.versioninfo:eu-repo/semantics/publishedVersiones
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.contributor.affiliationUniversidad de Sevilla. Departamento de Estomatologíaes
dc.relation.projectIDCTS113es
dc.identifier.doi10.1089/ars.2012.4892es
dc.contributor.groupUniversidad de Sevilla. CTS 113: Investigacion Etiologia y Patogenia Periodontal, Patologia Oral y Enfermedades Musculareses
idus.format.extent8es
dc.journaltitleAntioxidants and redox signalinges
dc.publication.volumen18es
dc.publication.issue7es
dc.publication.initialPage800es
dc.publication.endPage807es

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