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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:722.)
© 2001 American Heart Association, Inc.

Editorials

Adventitial Fibroblasts

Backstage Journeymen

Francis J. Miller, Jr

From the Department of Internal Medicine, University of Iowa, Iowa City.

Correspondence to Dr Francis J. Miller, Department of Internal Medicine, E314-4 GH, University of Iowa Hospitals, Iowa City, IA 52242. E-mail francis-miller@uiowa.edu

Key Words: adventitial fibroblasts

Although it has been 20 years since the acceptance of the endothelial layer as more than a hemostatic barrier in the blood vessel, the adventitia continues to be primarily considered a supporting structure, and its role in vascular disease has been easily dismissed. However, there is increasing support for the adventitia as a mediator of vascular dysfunction and a potential therapeutic target.^{1 2} In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Shi et al³ report elevated superoxide levels in coronary adventitial fibroblasts within 1 day of balloon injury. The source of superoxide appears to be NAD(P)H oxidase.

The observation that adventitial fibroblasts generate reactive oxygen species (ROS) in response to vessel injury is not necessarily surprising. After injury, growth factors and cytokines are released from platelets and cell debris. NAD(P)H oxidase expression and superoxide production in fibroblasts increase within hours after exposure to angiotensin II.⁴ If vessel injury is severe and there is medial disruption, adventitial cells are activated, whereas when injury is mild, without rupture of the internal elastic membrane, adventitial activation is modest.^{5 6} These observations suggest that in response to endoluminal injury, locally released substances activate fibroblasts.

How can cells in the adventitia, which are relatively distant from the endothelium and subendothelial space, contribute to vascular dysfunction and neointimal formation? The findings of Shi et al³ suggest that increased adventitial superoxide levels after balloon injury may modulate fibroblast growth. Redox-mediated events in activated fibroblasts, which may include the release of a variety of paracrine substances and the . . . [Full Text of this Article]

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