Figure 1.

Atherosclerosis involves apoB-containing lipoproteins. The atherosclerotic process begins with compromise of the endothelial barrier, allowing apoB-containing LDL cholesterol to migrate into the arterial intima. Activated endothelium fosters attachment, migration and proliferation of vascular smooth muscle cells (SMC) and macrophages. Retained apoB-containing lipoproteins are oxidatively modified within the vascular intima. Oxidized (ox)LDL contains protein components, creating a net negative charge, making the particles highly attractive to macrophages. Phagocytosis allows for the accumulation of lipids within macrophages, producing foam cells. OxLDL-laden foam cells amass and form the fatty streak and eventually the lumen-narrowing atheromatous plaque that restricts blood flow. Additionally, inflammatory signaling pathways are activated, leading to increased cell migration and LDL modification.