動脈硬化の発症機序(<特集>動脈硬化とアフェレシス)

概要

論文の詳細を見る
Atherosclerosis, previously considered to be a cholesterol storage disease, is currently understood as an inflammatory disease. The earliest change is subendothelial deposits of lipid and lipoprotein. The next event is the recruitment of inflammatory cells from the circulation. This process is mediated by adhesion molecules of which expression is enhanced both on leukocytes and endothelial cells by atherogenic risks. The leukocytes then transmigrate into subendotelial space, the intima. The monocytes exposed to modified LDL or cytokines there become converted to activated macrophages, take up modified lipoproteins and become foam cells. During these processes, activated endothelial cells and leukocytes secrete a variety chemokines and cytokines which further activate the cells in auto-or paracrine fashion and lead to the recruitment of smooth muscle cells from the media of the artery. If the conditions continue, the advanced lesion is developed, consisting of smooth muscle cells, macrophages, T-lymphocytes, lipid, necrotic cell debris and connective tissue covered by a fibrous cap formed by smooth muscle cells, elastic fibers and proteoglycans. Clinical events such as myocardial or cerebral infarction are mostly derived from the formation of an occlusive thrombus at the site of plaque rapture or erosion of the plaque surface.
日本アフェレシス学会の論文
2008-02-29