NADPH oxidase-mediated oxidative stress
Palabras clave : 
Hypertension
Membrane Transport Proteins/metabolism
NADPH Oxidase/metabolism
Oxidative Stress
Phosphoproteins/metabolism
Fecha de publicación: 
2005
Editorial : 
Mary Ann Liebert
ISSN: 
1557-7716
Cita: 
Zalba G, San Jose G, Moreno MU, Fortuno A, Diez J. NADPH oxidase-mediated oxidative stress: genetic studies of the p22(phox) gene in hypertension. Antioxid Redox Signal 2005 Sep-Oct;7(9-10):1327-1336.
Resumen
Increased vascular production of reactive oxygen species, especially superoxide anion, significantly contributes to the oxidative stress associated with hypertension. An enhanced superoxide production causes an increased inactivation of nitric oxide that diminishes nitric oxide bioavailability, thus contributing to endothelial dysfunction and hypertrophy of vascular cells. It has been shown that NADPH oxidases play a major role as the most important sources of superoxide anion in phagocytic and vascular cells. Several experimental observations have described an enhanced superoxide generation as a result of NADPH oxidase activation in hypertension. Although these enzymes respond to stimuli such as vasoactive factors, growth factors, and cytokines, recent data suggest a significant role of the genetic background in the modulation of the expression of its different components. Several polymorphisms have been identified in the promoter and in the coding region of CYBA, the gene that encodes the essential subunit of the NADPH oxidase p22phox, some of which seem to influence significantly the activity of these enzymes in the context of cardiovascular diseases. Among CYBA polymorphisms, genetic investigations have provided a novel marker, the -930(A/G) polymorphism, which determines the genetic susceptibility of hypertensive patients to oxidative stress.

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