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<dc:title>Use of Kv1.3 channel blockers for the prevention of restenosis in human vessels: Mechanisms and outcomes in diabetic patients</dc:title>
<dc:creator>Arévalo Martínez, Marycarmen</dc:creator>
<dc:contributor>Pérez García, María Teresa</dc:contributor>
<dc:contributor>Cidad Velasco, María Del Pilar</dc:contributor>
<dc:contributor>Universidad de Valladolid. Facultad de Medicina</dc:contributor>
<dc:subject>Kv1.5</dc:subject>
<dc:subject>Kv1.3</dc:subject>
<dc:subject>Diabetes</dc:subject>
<dc:subject>32 Ciencias Médicas</dc:subject>
<dc:description>Vascular smooth muscle cells (VSMCs) can undergo phenotypic&#xd;
modulation (PM) to a dedifferentiated state, which contributes to&#xd;
angiogenesis and vessel repair. PM is triggered by vascular surgeries such&#xd;
as those directed to unclog obstructed vessels. However, an excessive&#xd;
VSMC migration and proliferation drives intimal hyperplasia (IH) leading to&#xd;
restenosis. This situation is even worse in patients with background&#xd;
diseases like type 2 diabetes mellitus (T2DM). T2DM patients have more&#xd;
aggressive forms of vascular disease and worse outcomes, with&#xd;
exacerbated restenosis after vascular surgery.&#xd;
We have previously demonstrated that an increased functional expression&#xd;
of the potassium channel Kv1.3 contributes to PM in several models of&#xd;
VSMCs, as Kv1.3 blockers inhibit VSMCs migration and proliferation. In&#xd;
addition, we found that Kv1.3 increased activity upon PM is a consequence&#xd;
of Kv1.5 downregulation, so that the changes in Kv1.3 to Kv1.5 ratio can&#xd;
define VSMCs phenotype.</dc:description>
<dc:description>Departamento de Bioquímica y Biología Molecular y Fisiología</dc:description>
<dc:description>Doctorado en Investigación Biomédica</dc:description>
<dc:date>2020-11-16T13:18:45Z</dc:date>
<dc:date>2020-11-16T13:18:45Z</dc:date>
<dc:date>2020</dc:date>
<dc:type>info:eu-repo/semantics/doctoralThesis</dc:type>
<dc:type>info:eu-repo/semantics/publishedVersion</dc:type>
<dc:identifier>http://uvadoc.uva.es/handle/10324/43490</dc:identifier>
<dc:identifier>10.35376/10324/43490</dc:identifier>
<dc:language>eng</dc:language>
<dc:rights>Attribution-NonCommercial-NoDerivatives 4.0 Internacional</dc:rights>
<dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
<dc:rights>http://creativecommons.org/licenses/by-nc-nd/4.0/</dc:rights>
<dc:format>application/pdf</dc:format>
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