Abstract
Decades of research have increased our understanding of the role and interplay between serum cholesterol, inflammation, and oxidative stress in the pathogenesis of atherosclerosis (1). Uptake and retention of low-density lipoprotein (LDL) by macrophages in the intima is dependent on adhesion molecules and inflammatory cytokines and amplified by oxidative stress. This hostile environment is toxic to endothelial and smooth muscle cells, which further hampers vascular homeostasis. These interrelated steps provide potentially fruitful therapeutic targets for the prevention and treatment of atherosclerosis.