Statin-mediated monocyte apoptosis in the context of atherosclerosis. During formation of the atherosclerotic plaque monocytes are recruited and retained in the vascular wall, where they differentiate into macrophages. Macrophages incorporate lipids giving rise to foam cells, which exhibit a dysregulated phenotype possibly due to oxidative stress. Mature macrophages and foam cells are thought to promote plaque rupture by eroding the fibromuscular cap. This is likely achieved through release of matrix-degrading proteases and also via FasL-mediated cytotoxic effects on adjacent vascular smooth muscle cells. Statins modulate both primary vascular release of MCP-1 and monocyte chemotaxis. In situ monocyte apoptosis might also contribute to their downstream effects on plaque stability.