Figure 3.

Pathophysiology of early and advanced atherosclerosis. Upon transcytosis and oxidation of LDL, the endothelium becomes activated leading to leukocyte infiltration into the vessel wall. This triggers thickening of the intimal layer, ultimately resulting in foam cell accumulation and necrotic core formation. Hypoxia induces intra-plaque angiogenesis, but these neovessels are often mature which leads to intraplaque hemorrhage and excessive extravasation of leukocytes. This results in production of cytokines, growth factors and MMPs, creating a continuous loop of plaque growth and ultimately plaque rupture. Hb—hemoglobin; LDL—low-density lipoproteins; MMPs—metallo matrix proteinases; oxLDL—oxidized low-density lipoproteins; VSMC—vascular smooth muscle cell.