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    Por favor, use este identificador para citar o enlazar este ítem:http://uvadoc.uva.es/handle/10324/43490

    Título
    Use of Kv1.3 channel blockers for the prevention of restenosis in human vessels: Mechanisms and outcomes in diabetic patients
    Autor
    Arévalo Martínez, MarycarmenAutoridad UVA
    Director o Tutor
    Pérez García, María TeresaAutoridad UVA
    Cidad Velasco, María del Pilar
    Editor
    Universidad de Valladolid. Facultad de MedicinaAutoridad UVA
    Año del Documento
    2020
    Titulación
    Doctorado en Investigación Biomédica
    Resumo
    Vascular 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.
    Materias (normalizadas)
    Kv1.5
    Kv1.3
    Diabetes
    Materias Unesco
    32 Ciencias Médicas
    Departamento
    Departamento de Bioquímica y Biología Molecular y Fisiología
    DOI
    10.35376/10324/43490
    Idioma
    eng
    URI
    http://uvadoc.uva.es/handle/10324/43490
    Tipo de versión
    info:eu-repo/semantics/publishedVersion
    Derechos
    openAccess
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    • Tesis doctorales UVa [1988]
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    Nombre:
    TESIS-1756-201103 .pdf
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    5.991Mb
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    Attribution-NonCommercial-NoDerivatives 4.0 InternacionalExceto quando indicado o contrário, a licença deste item é descrito como Attribution-NonCommercial-NoDerivatives 4.0 Internacional

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