Abstract
Under physiological conditions human blood platelets play a beneficial role in fibrinolysis and regulate the balance with prostacyclin and other factors derived from the endothelium. In response to endothelial injury, adherence of platelets to the denuded arterial surface, platelet aggregation, release of mitogens and subsequent cell proliferation characterize early fibrous plaque lesions. 'Native' atherogenic plasma lipoproteins which are abundant in hypercholesterolemia have been found to play a subtle role in the development of atherosclerosis. In addition, lipoproteins modulate platelet function and alter the susceptibility of platelets to different stimulating agents. The properties of 'modified' atherogenic lipoproteins also seem to be well documented with respect to atherogenesis. After uptake by macrophages, modified atherogenic plasma lipoproteins are thought to contribute to formation of fatty streak lesions. On the other hand, modified atherogenic lipoproteins may directly promote endothelial injury and thus favour enhanced endothelial-platelet interactions. However, the direct effects of modified atherogenic lipoproteins on platelet function have not been revealed in detail. Recent findings have documented that activated platelets themselves may promote modification of atherogenic plasma lipoproteins and thus contribute to enhanced foam cell formation. Therefore stimulation of thrombocytes, and their interaction with native and modified lipoproteins must be considered an important factor in the current concept of atherogenesis.