Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:1962-1971
Published online before print October 24, 2002, doi: 10.1161/01.ATV.0000043452.30772.18
Published online before print October 24, 2002, doi: 10.1161/01.ATV.0000043452.30772.18
© 2002 American Heart Association, Inc.
Brief Reviews |
The Reactive Adventitia
Fibroblast Oxidase in Vascular Function
From the Hypertension and Vascular Research Division (P.J.P.), Henry Ford Hospital, Detroit, Michigan, and the Department of Microbiology (F.E.R.), University of Iowa, Iowa City.
Correspondence to Patrick J. Pagano, PhD, Room7044, E&R Building, Henry Ford Hospital, 2799 W Grand Blvd, Detroit, MI 48202-2689. E-mail ppagano1{at}hfhs.org
The vascular adventitia is activated in a variety of cardiovascular disease states and has recently been shown to be a barrier to nitric oxide bioactivity. Vascular fibroblasts produce substantial amounts of NAD(P)H oxidase–derived reactive oxygen species (ROS) that appear to be involved in fibroblast proliferation, connective tissue deposition, and perhaps vascular tone. However, the physiological and pathophysiological roles of the adventitia have not been extensively studied, possibly because of its location in large blood vessels remote from the vascular endothelium. In recent years, substantial information has been gathered on pathways leading to oxidase activation in smooth muscle cells and fibroblasts and the downstream signaling pathways leading to hypertrophy and proliferation. A clearer understanding of the molecular mechanisms involved will likely lead to therapeutic strategies aimed at preventing vascular dysfunction in diseases such as atherosclerosis, in which these pathways are activated.
Key Words: NAD(P)H oxidase • NADPH oxidoreductase • fibroblast • vascular smooth muscle • adventitia • remodeling
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