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dc.contributor.authorPosada Duque, Rafael Andrés-
dc.contributor.authorSampaio Barreto, George Emilio-
dc.contributor.authorCardona Gómez, Gloria Patricia-
dc.date.accessioned2022-02-07T21:01:54Z-
dc.date.available2022-02-07T21:01:54Z-
dc.date.issued2014-
dc.identifier.issn1662-5102-
dc.identifier.urihttp://hdl.handle.net/10495/25856-
dc.description.abstractABSTRACT: Neurological disorders are prevalent worldwide. Cerebrovascular diseases (CVDs), which account for 55% of all neurological diseases, are the leading cause of permanent disability, cognitive and motor disorders and dementia. Stroke affects the function and structure of blood-brain barrier, the loss of cerebral blood flow regulation, oxidative stress, inflammation and the loss of neural connections. Currently, no gold standard treatments are available outside the acute therapeutic window to improve outcome in stroke patients. Some promising candidate targets have been identified for the improvement of long-term recovery after stroke, such as Rho GTPases, cell adhesion proteins, kinases, and phosphatases. Previous studies by our lab indicated that Rho GTPases (Rac and RhoA) are involved in both tissue damage and survival, as these proteins are essential for the morphology and movement of neurons, astrocytes and endothelial cells, thus playing a critical role in the balance between cell survival and death. Treatment with a pharmacological inhibitor of RhoA/ROCK blocks the activation of the neurodegeneration cascade. In addition, Rac and synaptic adhesion proteins (p120 catenin and N-catenin) play critical roles in protection against cerebral infarction and in recovery by supporting the neurovascular unit and cytoskeletal remodeling activity to maintain the integrity of the brain parenchyma. Interestingly, neuroprotective agents, such as atorvastatin, and CDK5 silencing after cerebral ischemia and in a glutamate-induced excitotoxicity model may act on the same cellular effectors to recover neurovascular unit integrity. Therefore, future efforts must focus on individually targeting the structural and functional roles of each effector of neurovascular unit and the interactions in neural and non-neural cells in the post-ischemic brain and address how to promote the recovery or prevent the loss of homeostasis in the short, medium and long term.spa
dc.format.extent19spa
dc.format.mimetypeapplication/pdfspa
dc.language.isoengspa
dc.publisherFrontiers Mediaspa
dc.type.hasversioninfo:eu-repo/semantics/publishedVersionspa
dc.rightsinfo:eu-repo/semantics/openAccessspa
dc.rights.urihttp://creativecommons.org/licenses/by/2.5/co/*
dc.titleProtection after stroke : cellular effectors of neurovascular unit integrityspa
dc.typeinfo:eu-repo/semantics/articlespa
dc.publisher.groupGrupo de Neurociencias de Antioquiaspa
dc.identifier.doi10.3389/fncel.2014.00231-
oaire.versionhttp://purl.org/coar/version/c_970fb48d4fbd8a85spa
dc.rights.accessrightshttp://purl.org/coar/access_right/c_abf2spa
oaire.citationtitleFrontiers in Cellular Neurosciencespa
oaire.citationstartpage1spa
oaire.citationendpage19spa
oaire.citationvolume8spa
dc.rights.creativecommonshttps://creativecommons.org/licenses/by/4.0/spa
dc.publisher.placeLausana, Suizaspa
dc.type.coarhttp://purl.org/coar/resource_type/c_dcae04bcspa
dc.type.redcolhttps://purl.org/redcol/resource_type/ARTREVspa
dc.type.localArtículo de revisiónspa
dc.subject.decsAccidente Cerebrovascular-
dc.subject.decsStroke-
dc.subject.decsProteínas de Unión al GTP rho-
dc.subject.decsrho GTP-Binding Proteins-
dc.subject.proposalBBBspa
dc.subject.proposalP120 cateninspa
dc.description.researchgroupidCOL0010744spa
dc.relation.ispartofjournalabbrevFront. Cell. Neurosci.spa
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