Apoptosis is the physiologic mechanism of programmed cell death having a function opposite to mitosis in the control of tissue size. Angiogenesis is the process of new vessel formation from pre-existing blood vessels which participates in embryogenesis, tissue growth, endometrial regeneration and wound healing. The role of both apoptosis and angiogenesis in the development and evolution of neoplasia and atherosclerosis has been extensively studied. Factors such as high concentration of glucose, oxidized LDL and oxidative stress, which are important in the pathogenesis of atherosclerosis also stimulate apoptosis. Increased apoptosis of endothelial cells but mainly also of smooth muscle cells and macrophages within the atherosclerotic plaque results in plaque instability and predisposes to plaque rupture and thrombosis. Endothelial dysfunction, forming the biochemical basis for the subsequent evolution of atherosclerosis, is associated with the release of growth factors which not only induce endothelial and smooth muscle cell hyperplasia but are also responsible for angiogenesis in the neointima and the growth of the atherosclerotic plaque. Neovascularization has been found to be higher in ruptured plaques and in cases of unstable angina. Thus, plaque neovascularization seems to also be a factor predisposing to complications of atherosclerosis.

Key words: Atherosclerosis, apoptosis, angiogenesis.

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