FIG. 1.

Model of atherosclerotic plaque formation at sites of disturbed flow. While endothelial cells in areas of high flow show a quiescent and anti-inflammatory phenotype, the endothelium in regions of turbulent flow exhibits an activated phenotype, characterized by high levels of proinflammatory gene expression that facilitates monocyte recruitment. Monocyte-derived macrophages avidly engulf lipoprotein deposits and potentiate local inflammation. Inflammation in the vessel wall stimulates smooth muscle recruitment, enhancing fibrous cap formation and preventing plaque rupture and thrombogenesis.