[Recent pathophysiologic aspects of atherogenesis]

Although the causes for atherogenesis are multifactorial, derangements of the lipid- and lipoprotein metabolism play a key role for the development of early lesions. The major risk factor for atherosclerosis cholesterol is a substance necessary for life. Cholesterol may be synthesized by any living cell of the human body. In order to save body fuel, cells take up cholesterol from circulation. All plasma lipids are bound in the blood to specific apolipoproteins. Apo-B containing lipoproteins are capable in binding to specific cell surface receptors (B/E-R) and to ingest cholesterol into the cells. Under circumstances, where the binding affinity to the B/E-R is reduced, atherogenic lipoproteins accumulate in the plasma and are eventually cleared by the scavenger receptor. These mechanisms play a key role in atherogenesis. Apo-A containing lipoproteins in contrast are designed to shuttle deposited cholesterol from the periphery to the liver, where it is oxidized to bile acids. The role of the four cell types:endothelial- and smooth muscle cells, macrophages and thrombocytes for atherogenesis in the concert with pathophysiological events of the lipid metabolism are discussed, and genetic diseases are explained at a molecular level.