Publication: Regulación de la entrada de calcio en arterias de resistencia: papel de la fosfatidilinositol 3-kinasa (PI3K) y de las kinasas activadas por mitógenos (MAPK)
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2019-12-19
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Universidad Complutense de Madrid
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Abstract
La resistencia a la insulina produce la alteración de acciones vasculares que dependen de las vías de señalización de la PI3K/óxido nítrico (NO) y de la MAPK/Endotelina-1 (ET-1). Este desequilibrio desemboca en una contracción exacerbada y disfunción endotelial (Kim et al., 2006; Prieto et al., 2013). Sin embargo, las alteraciones de la homeostasis del calcio (Ca2+) en el músculo liso vascular (MLV) se asocian a vasoconstricción anormal y a complicaciones vasculares en enfermedades metabólicas (Okon et al., 2005, Ford et al., 2010; Villalba et al., 2011).En el MLV, la contracción depende del incremento en la concentración de Ca2+ intracelular ([Ca2+]i) debido a la entrada de Ca2+ extracelular y/o la movilización de Ca2+ de los almacenes del retículo sarcoplásmico (RS) seguido por la fosforilación de la cadena ligera de miosina (MLC) y la formación de los puentes cruzados de actina/ miosina (Liu & Khalil, 2018). Sin embargo, incrementos en la fuerza contráctil pueden ocurrir a una determinada [Ca2+]i, proceso denominado sensibilización al Ca2+ (Somlyo & Somlyo, 2003; Villalba et al., 2007)...
Insulin resistance states result in the impairment of insulin vascular actions that depend on PI3K/nitric oxide (NO) and MAPK/Endothelin-1 (ET-1) signaling pathways. This imbalance leads to an exacerbated vascular contraction and endothelial dysfunction (Kim et al., 2006; Prieto et al., 2013). However, alterations of calcium (Ca2+) homeostasis in vascular smooth muscle (VSM) are associated with abnormal vasoconstriction and vascular complications in metabolic disease (Okon et al., 2005, Ford et al., 2010; Villalba et al., 2011).In VSM, contraction depends on the elevation of intracellular Ca2+ concentration ([Ca2+]i) due to extracellular Ca2+ entry and/or Ca2+ mobilization from the stores in the sarcoplasmic reticulum followed by activation of myosin light chain (MLC) kinase, MLC phosphorylation and the subsequent formation of actin/myosin crossbridges (Liu & Khalil, 2018). However, increases in contractile force development can also occur at a given [Ca2+]i, a process mediated by Ca2+ sensitization mechanisms (Somlyo & Somlyo, 2003; Villalba et al., 2007)...
Insulin resistance states result in the impairment of insulin vascular actions that depend on PI3K/nitric oxide (NO) and MAPK/Endothelin-1 (ET-1) signaling pathways. This imbalance leads to an exacerbated vascular contraction and endothelial dysfunction (Kim et al., 2006; Prieto et al., 2013). However, alterations of calcium (Ca2+) homeostasis in vascular smooth muscle (VSM) are associated with abnormal vasoconstriction and vascular complications in metabolic disease (Okon et al., 2005, Ford et al., 2010; Villalba et al., 2011).In VSM, contraction depends on the elevation of intracellular Ca2+ concentration ([Ca2+]i) due to extracellular Ca2+ entry and/or Ca2+ mobilization from the stores in the sarcoplasmic reticulum followed by activation of myosin light chain (MLC) kinase, MLC phosphorylation and the subsequent formation of actin/myosin crossbridges (Liu & Khalil, 2018). However, increases in contractile force development can also occur at a given [Ca2+]i, a process mediated by Ca2+ sensitization mechanisms (Somlyo & Somlyo, 2003; Villalba et al., 2007)...
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Tesis inédita de la Universidad Complutense de Madrid, Facultad de Farmacia, Departamento de Fisiología, leída el 21-10-2019