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Título:
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The Crosstalk between Cardiac Lipotoxicity and Mitochondrial Oxidative Stress in the Cardiac Alterations in Diet-Induced Obesity in Rats
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Autores:
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Jiménez-González, Sara ;
Marín-Royo, Gema ;
Jurado-López, Raquel ;
Bartolome Pascual, Visitación ;
Romero Miranda, Ana ;
Luaces Méndez, María ;
Islas, Fabián ;
Nieto, María Luisa ;
Martínez Martínez, Ernesto ;
Cachofeiro Ramos, Victoria
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Tipo de documento:
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texto impreso
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Editorial:
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MDPI, 2020-02-17
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Dimensiones:
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application/pdf
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Nota general:
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cc_by
info:eu-repo/semantics/openAccess
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Idiomas:
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Palabras clave:
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Estado = Publicado
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Materia = Ciencias Biomédicas: Medicina: Cardiología
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Materia = Ciencias Biomédicas: Medicina: Fisiología
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Tipo = Artículo
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Resumen:
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The impact of the mitochondria-targeted antioxidant MitoQ was evaluated in the cardiac alterations associated with obesity. Male Wistar rats were fed either a high fat diet (HFD, 35% fat) or a standard diet (CT, 3.5% fat) for 7 weeks and treated with MitoQ (200 µM). The effect of MitoQ (5 nM) in rat cardiac myoblasts treated for 24 h with palmitic acid (PA, 200 µM) was evaluated. MitoQ reduced cardiac oxidative stress and prevented the development of cardiac fibrosis, hypertrophy, myocardial 18-FDG uptake reduction, and mitochondrial lipid remodeling in HFD rats. It also ameliorated cardiac mitochondrial protein level changes observed in HFD: reductions in fumarate hydratase, complex I and II, as well as increases in mitofusin 1 (MFN1), peroxisome proliferator-activated receptor gamma coactivator 1-alpha, and cyclophilin F (cycloF). In vitro, MitoQ prevented oxidative stress and ameliorated alterations in mitochondrial proteins observed in palmitic acid (PA)-stimulated cardiac myoblasts: increases in carnitine palmitoyltransferase 1A, cycloF, and cytochrome C. PA induced phosphorylation of extracellular signal-regulated kinases and nuclear factor-?B p65. Therefore, the data show the beneficial effects of MitoQ in the cardiac damage induced by obesity and suggests a crosstalk between lipotoxicity and mitochondrial oxidative stress in this damage.
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En línea:
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https://eprints.ucm.es/id/eprint/61794/1/cells-09-00451-v2.pdf
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