Adventitial Fibroblasts

Abstract

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, …