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dc.contributor.authorBolaños, Juan P.-
dc.contributor.authorCadenas, Enrique-
dc.contributor.authorDuchen, Michael R.-
dc.contributor.authorHampton, Mark B.-
dc.contributor.authorMann, Giovanni E.-
dc.contributor.authorMurphy, Michael P.-
dc.date.accessioned2017-11-07T08:14:51Z-
dc.date.available2017-11-07T08:14:51Z-
dc.date.issued2016-
dc.identifierdoi: 10.1016/j.freeradbiomed.2016.08.004-
dc.identifierissn: 0891-5849-
dc.identifiere-issn: 1873-4596-
dc.identifier.citationFree Radical Biology and Medicine 100: 1-4 (2016)-
dc.identifier.urihttp://hdl.handle.net/10261/157041-
dc.description.abstractMitochondria are functional entities that harbor the energy-conservation machinery that supports cell function through the coordination of mitochondrion-derived molecules involved in the regulation of cell signaling and transcription. Conversely, mitochondria are targets of an ever-increasing number of signaling pathways and their activity is also modulated by several transcription factors. The cell's energy-redox homeostasis is primarily a function of mitochondrial oxidative phosphorylation and the formation of O2.–/H2O2. Notably, other mitochondrion-driven processes contribute to cellular homeostasis, such as mitochondrial biogenesis and dynamics, mitochondrial quality control (autophagy and mitophagy), mitochondrial proteostasis and the role of the mitochondrial unfolded protein response (UPRmt), and redox signaling in the homeostatic control of mitochondrial function. This Free Radical Biology & Medicine special issue on Mitochondrial Redox Signaling in Health and Disease covers some aspects of the myriad of processes embraced by mitochondrial biology and physiology, provides mechanistic insights linking mitochondrial function with cell function, and recognizes mitochondrial function as an amenable therapeutic target.-
dc.description.sponsorshipG.E.M. acknowledges support from the British Heart Foundation (FS/13/66/30445, PG/13/1/29801 and Heart Research UK (Novel and Emerging Technologies Grant RG2633). E.C. acknowledges support from NIH grant RO1AG016718. M.R.D. acknowledges support from BBSRC grant (BB/L020874/1) and from Parkinson's UK (G1101).-
dc.publisherElsevier-
dc.relation.isversionofPostprint-
dc.rightsopenAccess-
dc.titleIntroduction to special issue on mitochondrial redox signaling in health and disease-
dc.typeartículo-
dc.identifier.doi10.1016/j.freeradbiomed.2016.08.004-
dc.relation.publisherversionhttps://doi.org/10.1016/j.freeradbiomed.2016.08.004-
dc.date.updated2017-11-07T08:14:52Z-
dc.description.versionPeer Reviewed-
dc.language.rfc3066eng-
dc.rights.licensehttp://creativecommons.org/licenses/by-nc-nd/4.0/-
dc.contributor.funderBiotechnology and Biological Sciences Research Council (UK)-
dc.contributor.funderParkinson's Disease Society (UK)-
dc.contributor.funderBritish Heart Foundation-
dc.contributor.funderNational Institutes of Health (US)-
dc.relation.csic-
dc.identifier.funderhttp://dx.doi.org/10.13039/501100000268es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100000274es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/100000002es_ES
dc.type.coarhttp://purl.org/coar/resource_type/c_6501es_ES
item.openairetypeartículo-
item.grantfulltextopen-
item.cerifentitytypePublications-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextWith Fulltext-
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