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Electron Microsc Rev. 1992;5(1):129-70.

Ultrastructure appearance of atherosclerosis in human and experimentally-induced animal models.

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Laboratory of Electron Microscopy, Saitama Medical School, Japan.


We describe here the basic structure of the aorta, the changes with aging and ultrastructural appearance of atherosclerosis of human and animal models. The architecture of the aortic wall is highly organized, for adaptation to changes of blood pressure. The main cells composing the vessel are endothelial cells and smooth muscle cells. They maintain the integrity and homeostasis of the aorta along with the extracellular matrix of collagen fibrils, elastic fibers and glycosaminoglycans. The structural changes with aging and atherogenesis are a compensative or degenerative phenomenon caused by many factors. Three major cells are the endothelial cell, smooth muscle cell and monocyte-derived macrophages (as well as platelets) all of which are involved in atherogenesis. Foam cells in atheromatous lesions are derived from macrophages and smooth muscle cells. Recently, the molecular biological nature and function of these cells and their derived-factors have been thoroughly investigated in cell culture and in experimental animal models caused by a mechanical injury of the endothelium or by a dietary induced hypercholesterolemia. However, the mechanism of the endothelial injury in vivo as well as formation of atheromatous cores of human atherosclerosis is not exactly understood. Some structural and functional changes inherent to the arterial wall during aging may play an important role in initiation or progression of human atherosclerosis.

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