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Reactive O2 species (ROS) are thought to contribute to the progression of atherosclerotic coronary artery disease (CAD).1 2 In this issue of Circulation Research , Cahilly and colleagues3 provide data supporting an association between a histidine72 to tyrosine mutation at the potential site for heme binding of the p22phox subunit of NAD(P)H oxidases and increased severity and progression of CAD in patients from the Lipoprotein and Coronary Atherosclerosis Study (LCAS). Although it was previously shown that the p22phox subunit of NAD(P)H oxidases is increased in atherosclerotic human coronary arteries,4 its precise role, if any, in disease pathogenesis and the impact of this mutation on the function of NAD(P)H oxidases remain to be elucidated. Given that the p22phox subunit is a component of both the phagocytic cell oxidase and NAD(P)H oxidases in other cell types in the vessel wall, the mutation could affect the production of ROS and multiple signaling systems that influence the progression of CAD.The best understood oxidase containing p22phox is the NADPH oxidase of phagocytic cells (eg, neutrophils and macrophages), which are known to contribute to the development and progression of atherosclerotic vascular disease. Activation of these phagocytic cells causes the cytosolic …

How Could a Genetic Variant of the p22 phox Component of NAD(P)H Oxidases Contribute to the Progression of Coronary Atherosclerosis?

How Could a Genetic Variant of the p22 ^phox Component of NAD(P)H Oxidases Contribute to the Progression of Coronary Atherosclerosis?