Quest for fire: seeking the source of pathogenic oxygen radicals in atherosclerosis

Abstract

There is an accumulating body evidence that atherosclerosis is either caused by or accompanied by oxidative events in the vessel wall. These oxidative events have been implicated in proatherogenic modification of proteins, alteration of gene expression, promotion of inflammation, remodeling of vessels, and perturbations of vascular tone. This body of literature has led to a dogma that oxidation is a prerequisite for the atherosclerotic process. In particular, oxidation of lipoproteins by activated macrophages in the subintimal space has been postulated to be an important early step in the atherosclerotic process.