Abstract
Oxidative stress plays a key role in the pathophysiology of several major cardiovascular diseases, including atherosclerosis, hypertension, heart failure, stroke, and diabetes. Reactive oxygen species (ROS) induce cardiovascular alterations by modulating cell contraction/dilatation, migration, growth/apoptosis, and extracellular matrix protein turnover, which contribute to vascular and cardiac remodeling. Of the several sources of ROS within the cardiovascular system, the family of the multisubunit NADPH oxidases appears to be a predominant contributor generating superoxide anions. Recent data suggest a significant role of the genetic background in NADPH oxidase regulation. Common genetic polymorphisms within CYBA, the gene that encodes the p22phox subunit of the NADPH oxidase, have been characterized in the context of cardiovascular diseases. This chapter aims to present the current state of research into these polymorphisms in their relationship to cardiovascular diseases.
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- ROS:
-
Reactive oxygen species
- •O2 – :
-
Superoxide
- CGD:
-
Chronic granulomatous disease
- SHR:
-
Spontaneously hypertensive rat
- CAD:
-
Coronary artery disease
- C/EBP:
-
CCAAT enhancer-binding protein
- HIF-1α:
-
Hypoxia-inducible factor-1alpha
- LD:
-
Linkage disequilibrium
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Acknowledgments
This work was supported by the agreement between the Foundation for Applied Medical Research and “UTE project CIMA”; European Union (InGenious HyperCare, LSHM-CT-2006-037093); Red Temática de Investigación Cooperativa en Enfermedades Cardiovasculares from the Instituto de Salud Carlos III, Ministry of Health (RD06/0014/0008) and Ministry of Science and Culture (SAF-2007-62553) of Spain.
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Zalba, G., Díez, J. (2010). Relationship of the CYBA Gene Polymorphisms with Oxidative Stress and Cardiovascular Risk. In: Sauer, H., Shah, A., Laurindo, F. (eds) Studies on Cardiovascular Disorders. Oxidative Stress in Applied Basic Research and Clinical Practice. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-60761-600-9_9
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