Atherosclerosis is the major cause of morbidity and mortality in the Western world, and its pathogenesis involves complicated interactions among cells of the arterial wall, blood cells, and plasma lipoproteins.12 The development of the atherosclerotic lesion involves a series of specific morphological, cellular, and molecular responses3 that can be considered inflammatory.4,5 Following endothelial injury, blood monocytes attach to the subendothelium and penetrate into the vessel wall, where they differentiate into macrophages, forming foam cells. Blood platelets at the site of the vascular injury, monocyte-derived macrophages, endothelial cells, and smooth muscle cells release mitogenic factors, which stimulate smooth muscle cell proliferation and migration. Smooth muscle cell proliferation in turn, together with the organization of thrombus and extracellular matrix synthesis, lead to the development of the atheromatous plaques. Macrophages, by releasing proteases such as collagenase and elastase, form an abscess in the plaque, which is covered by a thin fibrous cap. When this cap ruptures, a local thrombus is formed, and the degree and duration of thrombus formation, as well as the degree of collateral development, determines the fate of this thrombus.
Atherosclerosis is the result of multiple interactive risk factors, including hypertension, activation of blood platelets, increased plasma LDL-cholesterol level, and LDL oxidative modifications.678
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