Fig. 2

The pathology of atherothrombosis. Endothelial dysfunction causes activated endothelial cells to express inflammatory molecules, including VCAM-1 and ICAM-1. Monocytes interact with these inflammatory cell surface receptors and accumulate in the intima of blood vessels. Monocytes differentiate into lipid-loaded macrophages: LDL is taken up by macrophages and vascular SMCs leading to the formation of foam cells and the development of plaques. Accumulating and apoptotic foam cells form a necrotic core. The growing necrotic core eventually disrupts the fibrous cap and the leaking content of the plaques induces thrombosis through a series of reactions such as activation of platelets and the initiation of coagulation