Molecular mechanism of plaque formation in the artery

Low density lipoprotein (LDL) cholesterol enters dysfunctional endothelium (which is damaged by smoking or diabetes, for example, and this is reflected by decreased nitric oxide (NO) production) and is oxidized by macrophage and smooth muscle cells. Release of growth factors and cytokines, and upregulation of adhesion molecules, attracts further monocytes. Foam cells (arising from lipid-laden macrophages) accumulate and smooth muscle cells proliferate, which results in the growth of the plaque. Inflammatory cell infiltration, smooth muscle cell death through apoptosis, and matrix degradation through proteolysis (by matrix metalloproteinases- MMPs) generate a vulnerable plaque with a thin fibrous cap and a lipid-rich necrotic core. Plaque rupture can cause thrombosis which might be sufficient to cause vessel occlusion (or blockage).