This slide shows the pathogenesis of atherosclerosis. It starts from bad cholesterol or LDL particles enter through the gap between endothelial cells of blood vessel to intima layer. Then LDL particle will be modified by oxidation or glycation processes. The modified LDL will be recognized by macrophages as a foreign substance and should be destroyed. Macrophages will phagocytose this modified LDL without feedback mechanism. Then macrophages will become a foam cell and finally die and release many substances that can destroy the vessel. The accumulation of foam cells and other clotting component such as fibrous calcium which called plaque would make an atery thicken.