Abstract
1-3 . Atherosclerosis is a major cause of the morbidity and mortality associated with myocardial infarction and cerebral bleeding 4 . Intimal thickening with lipid depo‑ sition affects the elastic properties and contributes to the hydrophobic changes that occur in the intima of arteries. The anisotropic elasticity induced by micro‑ elastic changes is associated with functional distur‑ bances of the vascular wall 5 . In the atheromatous lesion infiltrated macrophages lymphocytes and platelets produce various kinds of cytokines and growth factors 6 . These cytokines and growth factors are synthesized by vascular cells such as the endothelial and smooth muscle cells and induce the inflammatory‑fibroproliferative response that is associated with cell proliferation and the production of extracellular matrix( ECM ) 7 . Proliferated smooth muscle cells induce local changes in the production of extracellular matrix components and may contribute to local weakening of the fibrous cap 8 . In the review presented here we discuss the mechanisms underly‑ ing the devolopment and fragility of atherosclerosis. 1.The role of endothelial dysfunction in athero‑ sclerosis Normal endothelial cells synthesize prostacyclin plasminogen activator factor VIII including the von Willebrand factor and various other components 1 .
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