At high magnification the necrotic center of an aortic atheroma shows foam cells (□) and cholesterol clefts (▪). In the process of atheroma formation, endothelial injury leads to increased permeability, leukocyte adhesion, and release of cytokines that attract blood monocytes, which transform into tissue macrophages that accumulate lipids, becoming foam cells. Macrophages readily ingest oxidized LDL cholesterol through their scavenger receptors. Macrophages also generate cytokines, driving cellular recruitment. An increased serum LDL increases the amount of oxidized LDL, promoting this process. In contrast, HDL cholesterol tends to promote mobilization of lipid in an atheroma and transport out to the liver.