Impairment of Cellular Interactions in the Arterial Wall: Arteriosclerosis

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Abstract
Our understanding of the cellular interactions in the arterial wall has increased considerably during the last 15 years. It has become clear that arteriosclerosis is a multifaceted disease, in which the accumulation of monocyte-derived macrophages, smooth muscle cells, T-lymphocytes, and lipid deposits contributes to the progressive thickening of the arterial intima. Many different types of stress, including cholesterol-rich lipoproteins, smoking, hypertension, hyperfibrinogenemia, endothelial damage, and inflammatory activation, contribute to this derailed "repair" response in the arterial intima. They are recognized as risk factors for cardiovascular disease. As a consequence of the progressive thickening of the arterial intima, the arterial lumen narrows, the barrier, vasoregulatory, and anticoagulant properties of the endothelium become impaired, and the arterial wall becomes prone to rupture and thrombosis. The advanced lesions can cause serious complications: myocardial infarction, stroke, claudication, and angina pectoris. As the extent of arteriosclerosis increases with age--a process that is accelerated by risk factors--it has a particular impact on the mortality and the quality of life of elderly people.

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