Figure 4.

Atherome plaque development. Accumulated LDL particles cross endothelial barrier and get oxidized in subendothelial space. Lipoprotein oxidation activates endothelial cells that increase the synthesis and secretion of chemoattractants and adhesion molecules promoting monocyte recruitment and transedothelial migration. Once at sub-endothelial compartments they are differentiated into machrophages and start to internalize ox-LDL through a non regulated SR-B1 scavenger receptor. Cholesterol excess in macrophages induces foam cell formation and promotes SVMC migration and fibrous cap synthesis. Finally, due to increased macrophage death and impaired efferocytosis, the size of the plaque increases and the diameter of the artery is reduced.