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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:919.)
© 2003 American Heart Association, Inc.

Editorials

c-Src and Smooth Muscle NAD(P)H Oxidase

Assembling a Path to Hypertrophy

M. Eugenia Cifuentes; Patrick J. Pagano

From the Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, Mich.

Correspondence to Dr Patrick Pagano, Henry Ford Hospital, Hypertension and Vascular Research Division, Room 7044, E&R Bldg, 2799 W Grand Blvd, Detroit, MI 48202-2689. E-mail ppagano1@hfhs.org

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Early studies of NAD(P)H oxidase in vascular tissue focused on the regulation of this complex enzyme and suggested its deleterious role in end-organ damage in hypertension and atherosclerosis.^1,2 The preponderance of data regarding the regulation of this enzyme and its similarity to the phagocyte prototype that mediates antimicrobial properties contributed to an impression that NAD(P)H oxidase played a similar toxic role in the vascular wall. Increasingly, reports challenge this notion and ascribe a very different role to the oxidase and ROS, demonstrating participation by angiotensin II–induced superoxide anion (O₂^-) in central nervous system signaling, and NAD(P)H oxidase as a critical player in growth factor–induced angiogenesis.^3,4

See page 981

Significant strides have been made recently in our understanding of the regulation of cardiovascular NAD(P)H oxidases, revealing elaborate control of these low-capacity NAD(P)H oxidases as generators of important signaling agents in cardiovascular disease including O₂^- and hydrogen peroxide (H₂O₂). At the focus of the discussion, endothelial and adventitial cells appear to contain a functional phagocyte-like NAD(P)H oxidase including p22^phox, gp91^phox, p47^phox, and p67^phox.^5–7 In contrast, vascular smooth muscle cells (VSMCs) appear to vary substantially in terms of the existence of homologues of gp91^phox (nox-1 and nox-4) and the absence of p67^phox.^8–10 The upregulation of vascular p22^phox, p47^phox, p67^phox, and nox-2 has suggested that active de novo synthesis and assembly occur during hormonal stimulation.^8,11,12 Angiotensin II (AngII) has been shown to cause phosphorylation and translocation of p47^phox in VSMCs, resulting in enhanced . . . [Full Text of this Article]

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