Título:
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Nox2 upregulation and p38? mapk activation in right ventricular hypertrophy of rats exposed to long-term chronic intermittent hypobaric hypoxia
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Autores:
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Pena, E. ;
Siques, P. ;
Brito, J. ;
Arribas, S.M. ;
Böger, R. ;
Hannemann, J. ;
León-Velarde, F. ;
González, M.C. ;
López, M.R. ;
de Pablo, Á.L.L.
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Tipo de documento:
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texto impreso
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Editorial:
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MDPI AG, 2020-12-14T16:10:03Z
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Nota general:
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info:eu-repo/semantics/restrictedAccess
https://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
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Idiomas:
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Inglés
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Palabras clave:
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Resumen:
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One of the consequences of high altitude (hypobaric hypoxia) exposure is the development of right ventricular hypertrophy (RVH). One particular type of exposure is long-term chronic intermittent hypobaric hypoxia (CIH); the molecular alterations in RVH in this particular condition are less known. Studies show an important role of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex-induced oxidative stress and protein kinase activation in different models of cardiac hypertrophy. The aim was to determine the oxidative level, NADPH oxidase expression and MAPK activation in rats with RVH induced by CIH. Male Wistar rats were randomly subjected to CIH (2 days hypoxia/2 days normoxia; n = 10) and normoxia (NX; n = 10) for 30 days. Hypoxia was simulated with a hypobaric chamber. Measurements in the RV included the following: hypertrophy, Nox2, Nox4, p22phox, LOX-1 and HIF-1? expression, lipid peroxidation and H2 O2 concentration, and p38? and Akt activation. All CIH rats developed RVH and showed an upregulation of LOX-1, Nox2 and p22phox and an increase in lipid peroxidation, HIF-1? stabilization and p38? activation. Rats with long-term CIH-induced RVH clearly showed Nox2, p22phox and LOX-1 upregulation and increased lipid peroxidation, HIF-1? stabilization and p38? activation. Therefore, these molecules may be considered new targets in CIH-induced RVH. © 2020, MDPI AG. All rights reserved.
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En línea:
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http://repositorio.upch.edu.pe/handle/upch/8760
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