Abstract
The progression and rupture of atherosclerotic plaques appear to play key rotes in the pathogenesis of ischemic coronary heart disease and ischemic stroke in humans. Recent research has suggested the importance of oxidative modification of low density lipoprotein (LDL). Oxidized LDL elicits lipid accumulation, as well as proin-flammatory changes, in arterial walls. Interactions between oxidized LDL and its receptors, such as scavenger receptor class A (SR-A), CD36, lectin-like oxidized LDL receptor-1 (LOX-1), and scavenger receptor for phos phatidylserine and oxidized lipoprotein (SR-PSOX), appear to play important roles in this process. In addition, the HDL-mediated efflux of cholesterol acts as protection against the oxidized LDL-induced atherogenesis. On the other hand, restenosis after angioplasty or surgery may depend more upon smooth muscle proliferation and extra-cellular matri production.
