[Molecular mechanisms in atherogenesis]

Disturbances of the lipid metabolism play a key role in atherogenesis, cholesterol, however, is not stored passively in the arterial wall, but on the basis of complex, partly still unknown humoral and cellular processes. The proliferative lesion of the arteriosclerotic vascular wall is characterized by injured endothelial cells, differentiating macrophages, immunocompetent T-lymphocytes and proliferating smooth muscle cells. Molecular biological investigations on cells of arteriosclerotic plaques among others clarified growth factors, cytokines, factors of angiogenesis and growth inhibitors in form and significance. Risk factors damage the endothelium and thus cause the production of these mediators. The adhesion proteins and the proto-oncogene c-sis play a further role. The latter might produce a connection between arteriosclerosis and cancer research.