Fig. 1.

Process of atherosclerotic lesion development. 1 Monocytes circulate in the circulation in a healthy vessel. 2 Endothelial dysfunction leads to the expression of cell adhesion molecules such as VCAM-1 by activated endothelial cells. These cell adhesion molecules allow monocytes to adhere to the wall and infiltrate to the tunica intima. 3 Monocytes differentiate into macrophages and engulf cholesterol-rich lipoproteins, becoming foam cells. 4 Smooth muscle cells (SMCs) infiltrate and stimulate the production of extracellular matrix components. 5 Foam cells and smooth muscle cells release matrix degrading matrix metalloproteinases (MMPs). 6 Degradation of the extracellular matrix (ECM) by MMPs increases plaque vulnerability to rupture and thrombus formation