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Articles by Cidad Velasco
A new therapeutical target for vascular diseases
Título Kv1.3 channels and vascular smooth muscle phenotypic modulation: A new therapeutical target for vascular diseases Titulación Doctorado en Investigación Biomédica Resumen Materias (normalizadas) Materias Unesco 2411.03 Fisiología Cardiovascular Palabras Clave Vascular remodeling Kv1.3 Remodelado vascular Kv1.3 Departamento Escuela de Doctorado Tipo de versión info:eu-repo/semantics/publishedVersion Derechos embargoedAccess
Kv1.3 channels modulate human vascular smooth muscle cells proliferation independently of mTOR signaling pathway
Phenotypic modulation (PM) of vascular smooth muscle cells (VSMCs) is central to the process of intimal hyperplasia which constitutes a common pathological lesion in occlusive vascular diseases. Changes in the functional expression of Kv1.5 and Kv1.3 currents upon PM in mice VSMCs have been found to contribute to cell migration and proliferation.
miR-126 contributes to the epigenetic signature of diabetic vascular smooth muscle and enhances antirestenosis effects of Kv1.3 blockers
Por favor, use este identificador para citar o enlazar este ítem:https://uvadoc.uva.es/handle/10324/65766 Título miR-126 contributes to the epigenetic signature of diabetic vascular smooth muscle and enhances antirestenosis effects of Kv1.3 blockers Documento Fuente Mol Metab . 2021 Nov:53:101306. doi: 10.1016/j.molmet.2021.101306. Epub 2021 Jul 20. Resumen Tipo de versión info:eu-repo/semantics/publishedVersion
miR-126 contributes to the epigenetic signature of diabetic vascular smooth muscle and enhances antirestenosis effects of Kv1.3 blockers
Por favor, use este identificador para citar o enlazar este ítem:https://uvadoc.uva.es/handle/10324/65715 Título miR-126 contributes to the epigenetic signature of diabetic vascular smooth muscle and enhances antirestenosis effects of Kv1.3 blockers Documento Fuente Mol Metab . 2021 Nov:53:101306. doi: 10.1016/j.molmet.2021.101306. Epub 2021 Jul 20. Resumen Tipo de versión info:eu-repo/semantics/publishedVersion
Kv channels and vascular smooth muscle cell proliferation
Kv channels are present in virtually all VSMCs and strongly influence contractile responses. However, they are also instrumental in the proliferative, migratory, and secretory functions of synthetic, dedifferentiated VSMCs upon PM. In fact, Kv channels not only contribute to all these processes but also are active players in the phenotypic switch itself.
Phenotypic Modulation of Cultured Primary Human Aortic Vascular Smooth Muscle Cells by Uremic Serum
Patients with chronic kidney disease (CKD) have a markedly increased incidence of cardiovascular disease (CVD). The high concentration of circulating uremic toxins and alterations in mineral metabolism and hormone levels produce vascular wall remodeling and significant vascular damage. Medial calcification is an early vascular event in CKD patients and is associated to apoptosis or necrosis and trans-differentiation of vascular smooth muscle cells (VSMC) to an osteogenic phenotype.
Kv1.3 Channel Inhibition Limits Uremia-Induced Calcification in Mouse and Human Vascular Smooth Muscle
Chronic kidney disease (CKD) significantly increases cardiovascular risk. In advanced CKD stages, accumulation of toxic circulating metabolites and mineral metabolism alterations triggers vascular calcification, characterized by vascular smooth muscle cell (VSMC) transdifferentiation and loss of the contractile phenotype. Phenotypic modulation of VSMC occurs with significant changes in gene expression.
Kv1.3 blockade inhibits proliferation of vascular smooth muscle cells in vitro and intimal hyperplasia in vivo
The modulation of voltage-gated K+ (Kv) channels, involved in cell proliferation, arises as a potential therapeutic approach for the prevention of intimal hyperplasia present in in-stent restenosis (ISR) and allograft vasculopathy (AV). We studied the effect of PAP-1, a selective blocker of Kv1.3 channels, on development of intimal hyperplasia in vitro and in vivo in 2 porcine models of vascular injury.
An in vitro and in vivo study
Por favor, use este identificador para citar o enlazar este ítem:https://uvadoc.uva.es/handle/10324/65357 Título Elastin-like recombinamer-based devices releasing Kv1.3 blockers for the prevention of intimal hyperplasia: An in vitro and in vivo study Documento Fuente Acta Biomater . 2020 Oct 1:115:264-274. doi: 10.1016/j.actbio.2020.07.053. Epub 2020 Aug 6. Resumen Tipo de versión info:eu-repo/semantics/acceptedVersion
Voltage‐dependent conformational changes of Kv1.3 channels activate cell proliferation
The voltage-dependent potassium channel Kv1.3 has been implicated in proliferation in many cell types, based on the observation that Kv1.3 blockers inhibited proliferation. By modulating membrane potential, cell volume, and/or Ca2+ influx, K+ channels can influence cell cycle progression. Also, noncanonical channel functions could contribute to modulate cell proliferation independent of K+ efflux.
Kv1.3 potassium channels and proliferation
Kv1.3 channels are involved in the switch to proliferation of normally quiescent cells, being implicated in the control of cell cycle in many different cell types and in many different ways. They modulate membrane potential controlling K + fluxes, sense changes in potential, and interact with many signaling molecules through their intracellular domains. From a mechanistic point of view, we can describe the role of Kv1.3 channels in proliferation with at least three different models.
miR-126 contributes to the epigenetic signature of diabetic vascular smooth muscle and enhances antirestenosis effects of Kv1.3 blockers
Objectives Vascular occlusive disease is a leading cause of death and disability worldwide. One of the major barriers of the current surgical therapeutic approaches is restenosis of the target vessel due to dedifferentiation of the vascular smooth muscle cells (VSMCs). Type 2 diabetes (T2DM) has a major impact on restenosis, with patients exhibiting more aggressive forms of vascular disease and poorer outcomes after surgery. The potassium channel, Kv1.3, is a critical player in VSMC proliferation.
Vascular smooth muscle ion channels in essential hypertension
Por favor, use este identificador para citar o enlazar este ítem:https://uvadoc.uva.es/handle/10324/65327 Título Vascular smooth muscle ion channels in essential hypertension Documento Fuente Front Physiol . 2022 Sep 23:13:1016175. doi: 10.3389/fphys.2022.1016175. Resumen Tipo de versión info:eu-repo/semantics/publishedVersion
Caracterización del perfil de expresión de canales iónicos en un modelo de diabetes
Título Caracterización del perfil de expresión de canales iónicos en un modelo de diabetes Titulación Grado en Química Resumen Palabras Clave Diabetes tipo 2 Macrófagos Canal de potasio Kv1.3 Departamento Departamento de Bioquímica y Biología Molecular y Fisiología
Mecanismos neurofisiológicos implicados en las alteraciones visuales de la migraña
Por favor, use este identificador para citar o enlazar este ítem:https://uvadoc.uva.es/handle/10324/63109 Título Mecanismos neurofisiológicos implicados en las alteraciones visuales de la migraña Titulación Grado en Óptica y Optometría Resumen Palabras Clave Migraña Sintomatología visual Aura migrañosa Departamento Departamento de Bioquímica y Biología Molecular y Fisiología Formato: Adobe PDF La licencia del ítem se describe como Attribution-NonCommercial-NoDerivatives 4.0 Internacional
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