Figure 1.

Model of atherogenesis. This scheme illustrates the development of an atherosclerotic plaque from left to right in a longitudinal section of an arterial vessel. (1) Upon activation by metabolic or inflammatory triggers, endothelial cells express adhesion molecules (Ad. mol.) that promote the recruitment of immune cells, such as blood monocytes (Mono). These cells then infiltrate the arterial intima, where monocyte differentiate into macrophages (Macro) and interact with other immune cells, such as neutrophils (Neutro) and T cells. (2) Increased uptake of modified lipoproteins via scavenger receptors or decreased cholesterol efflux accelerates the accumulation of intracellular free cholesterol and cholesteryl ester-loaded lipid droplets that promote foam cell formation. (3) Macrophage foam cells eventually die and fall apart, thereby forming a necrotic core. (4) Advanced, vulnerable plaques can rupture and thereby form an arterial thrombus, which can lead to a myocardial infarction or stroke. RBC, red blood cell; VSMC, vascular smooth muscle cell.