Abstract
Much interest has been generated recently concerning the role of reactive oxygen species (ROS) in vascular health and disease. The original “oxidative modification hypothesis of atherosclerosis” put forth in the early 1980’s by Steinberg and colleagues suggested that oxidative modification of LDL enhanced its atherogenic properties. An explosion of articles in this area substantiated the role of oxidized LDL in atherosclerosis (reviewed by Chisolm and Steinberg1), but recent work has expanded this hypothesis to include a role for free radicals in hypertension,2 the processes leading to restenosis after balloon angioplasty,3 vascular inflammation,4 diabetic vascular disease,5 and angiogenesis.6 Perhaps more importantly, ROS are essential to the normal functioning of the vessel wall, including endothelium-dependent relaxation, contraction, and the smooth muscle cell and endothelial cell growth and survival involved in repair and remodeling of the vessel wall. These diverse and critical roles of ROS in vascular physiology and pathophysiology make …
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