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dc.contributor.advisorPérez García, María Teresa es
dc.contributor.advisorCidad Velasco, María del Pilares
dc.contributor.authorArévalo Martínez, Marycarmen 
dc.contributor.editorUniversidad de Valladolid. Facultad de Medicina es
dc.date.accessioned2020-11-16T13:18:45Z
dc.date.available2020-11-16T13:18:45Z
dc.date.issued2020
dc.identifier.urihttp://uvadoc.uva.es/handle/10324/43490
dc.description.abstractVascular smooth muscle cells (VSMCs) can undergo phenotypic modulation (PM) to a dedifferentiated state, which contributes to angiogenesis and vessel repair. PM is triggered by vascular surgeries such as those directed to unclog obstructed vessels. However, an excessive VSMC migration and proliferation drives intimal hyperplasia (IH) leading to restenosis. This situation is even worse in patients with background diseases like type 2 diabetes mellitus (T2DM). T2DM patients have more aggressive forms of vascular disease and worse outcomes, with exacerbated restenosis after vascular surgery. We have previously demonstrated that an increased functional expression of the potassium channel Kv1.3 contributes to PM in several models of VSMCs, as Kv1.3 blockers inhibit VSMCs migration and proliferation. In addition, we found that Kv1.3 increased activity upon PM is a consequence of Kv1.5 downregulation, so that the changes in Kv1.3 to Kv1.5 ratio can define VSMCs phenotype.es
dc.description.sponsorshipDepartamento de Bioquímica y Biología Molecular y Fisiologíaes
dc.format.mimetypeapplication/pdfes
dc.language.isoenges
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectKv1.5es
dc.subjectKv1.3es
dc.subjectDiabeteses
dc.titleUse of Kv1.3 channel blockers for the prevention of restenosis in human vessels: Mechanisms and outcomes in diabetic patientses
dc.typeinfo:eu-repo/semantics/doctoralThesises
dc.description.degreeDoctorado en Investigación Biomédicaes
dc.identifier.doi10.35376/10324/43490
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersiones
dc.subject.unesco32 Ciencias Médicases


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