Figure 1.

Atherosclerosis begins with endothelial cell activation. The normal arterial wall contains a three-layered structure, with the intima consisting of wellarranged endothelial cells that perform important physiological functions. Endothelial cells normally have anti-inflammatory, anti-proliferative, and antioxidant status. When subjected to shear stress, the endothelium is activated, allowing large numbers of monocytes and LDL to enter the endothelium. In the endothelium, LDL is oxidized, amongst other modifications, and is, in turn, engulfed by macrophages formed by monocyte differentiation to form foam cells. Foam cells secrete pro-inflammatory factors, which promote endothelial cell-expressed ICAM and VCAM-mediated monocyte recruitment, creating a malignant closed loop. Finally, the apoptotic cells and lipids form a necrotic core, accompanied by smooth muscle cells that migrate over the necrotic core to form a fibrous cap. LDL, low-density lipoprotein; ICAM, intercellular cell adhesion molecule-1; VCAM, vascular cell adhesion molecule.