NADPH oxidase CYBA polymorphisms, oxidative stress and cardiovascular diseases.
Oxidative stress plays a key role in the pathophysiology of several major cardiovascular diseases, including atherosclerosis, hypertension, heart failure, stroke and diabetes. ROS (reactive oxygen species) affect multiple tissues either directly or through NO depletion. ROS induce cardiovascular dysfunction by modulating cell contraction/dilation, migration, growth/apoptosis and extracellular matrix protein turnover, which contribute to vascular and cardiac remodelling. Of the several sources of ROS within the cardiovascular system, a family of multisubunit NADPH oxidases appears to be a predominant contributor of superoxide anion. Recent findings suggest a significant role of the genetic background in NADPH oxidase regulation. Common genetic polymorphisms within the promoter and exonic sequences of CYBA, the gene that encodes the p22(phox) subunit of NADPH oxidase, have been characterized in the context of cardiovascular diseases. This review aims to present the current state of research into these polymorphisms in their relationship to cardiovascular diseases.
San José
Gorka
G
Division of Cardiovascular Sciences, Centre for Applied Medical Research, School of Medicine, University of Navarra, 31008 Pamplona, Spain.
Fortuño
Ana
A
Beloqui
Oscar
O
Díez
Javier
J
Zalba
Guillermo
G
D002318:Cardiovascular Diseases / Q000201:enzymology / Q000235:genetics* / Q000503:physiopathology; D006801:Humans; D019255:NADPH Oxidases / Q000235:genetics* / Q000502:physiology; D018384:Oxidative Stress / Q000235:genetics*; D011110:Polymorphism, Genetic
D019255:NADPH Oxidases; C086986:CYBA protein, human