Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/52825
Full metadata record
DC FieldValueLanguage
dc.contributor.authorRodríguez Allué, Manuel José-
dc.contributor.authorMartinez-Moreno, M.-
dc.contributor.authorOrtega González, Fco. Javier-
dc.contributor.authorMahy Gehenne, Josette Nicole-
dc.date.accessioned2014-03-24T08:55:12Z-
dc.date.available2014-03-24T08:55:12Z-
dc.date.issued2013-06-16-
dc.identifier.issn1942-0900-
dc.identifier.urihttp://hdl.handle.net/2445/52825-
dc.description.abstractNeurodegeneration is a complex process involving different cell types and neurotransmitters. A common characteristic of neurodegenerative disorders is the occurrence of a neuroinflammatory reaction in which cellular processes involving glial cells, mainly microglia and astrocytes, are activated in response to neuronal death. Microglia do not constitute a unique cell population but rather present a range of phenotypes closely related to the evolution of neurodegeneration. In a dynamic equilibrium with the lesion microenvironment, microglia phenotypes cover from a proinflammatory activation state to a neurotrophic one directly involved in cell repair and extracellular matrix remodeling. At each moment, the microglial phenotype is likely to depend on the diversity of signals from the environment and of its response capacity. As a consequence, microglia present a high energy demand, for which the mitochondria activity determines the microglia participation in the neurodegenerative process. As such, modulation of microglia activity by controlling microglia mitochondrial activity constitutes an innovative approach to interfere in the neurodegenerative process. In this review, we discuss the mitochondrial KATP channel as a new target to control microglia activity, avoid its toxic phenotype, and facilitate a positive disease outcome.-
dc.format.extent13 p.-
dc.format.mimetypeapplication/pdf-
dc.language.isoeng-
dc.publisherHindawi-
dc.relation.isformatofReproducció del document publicat a: http://dx.doi.org/10.1155/2013/194546-
dc.relation.ispartofOxidative Medicine and Cellular Longevity, 2013, vol. 2013, p. 194546-
dc.relation.urihttp://dx.doi.org/10.1155/2013/194546-
dc.rightscc-by (c) Rodríguez Allué et al., 2013-
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es-
dc.subject.classificationMicròglia-
dc.subject.classificationCanals de potassi-
dc.subject.classificationMalalties neurodegeneratives-
dc.subject.classificationMitocondris-
dc.subject.otherMicroglia-
dc.subject.otherPotassium channels-
dc.subject.otherNeurodegenerative diseases-
dc.subject.otherMitochondria-
dc.titleTargeting microglial KATP channels to treat neurodegenerative diseases: a mitochondrial issueeng
dc.typeinfo:eu-repo/semantics/article-
dc.typeinfo:eu-repo/semantics/publishedVersion-
dc.identifier.idgrec626710-
dc.date.updated2014-03-24T08:55:12Z-
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess-
Appears in Collections:Articles publicats en revistes (Ciències Fisiològiques)

Files in This Item:
File Description SizeFormat 
626710.pdf7.46 MBAdobe PDFView/Open


This item is licensed under a Creative Commons License Creative Commons