Atherosclerosis and its major complication, coronary heart disease, represent the major cause of death in industrialized nations. No single biochemical abnormality responsible for the initiation of the disease process has been identified. There are, however, a number of factors that increase the risk of developing the disease, including hypertension, hyperlipidemia, smoking, diabetes and personality type. Having more than one risk factor increases the chances of developing atherosclerosis. The first step in the genesis of atherosclerosis is thought to involve injury to the endothelial lining. The injury may result from hypertension or from inflammatory substances released from platelets. In response to this injury, smooth muscle cells synthesize extracellular materials to repair the injured vascular wall and there are no further complications. However, with repeated injury and infiltration of plasma lipoproteins and platelet factors, there may be proliferation of smooth muscle cells in both the intimal and medial portions of the wall. Continued proliferation leads to intimal thickening and to the appearance of cholesterol and cholesteryl esters. The major cholesteryl ester in atherosclerotic fibrous plaque is cholesteryl linoleate and is derived from plasma low density lipoprotein. In advanced lesions, there is a marked accumulation of extracellular lipids, mucopolysaccharides, and collagen. The smooth muscle cell plays a major role in the synthesis of these extracellular components. The final event in the atherosclerotic process involves rupture of the necrotic plaque and may lead to thrombus formation, occlusion and many of the clinical manifestations of the disease, including myocardial infarction, stroke and death.
|Translated title of the contribution||Biochemistry of atherosclerosis|
|Number of pages||20|
|State||Published - Jan 1 1974|
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