ABSTRACT
Platelets are blood cell fragments that originate from the cytoplasm of megakaryocytes in the bone marrow and circulate in blood. Although platelets were once considered to be merely passive participants in the coagulation cascade – just anucleate cells with a transient existence – they are now recognized as active synthesizers of humoral factors that potentiate both clot formation and inflammation. Platelets play a major role in the hemostatic process and in thrombus formation after an endothelial injury. Recent studies have provided insight into their functions in the onset of acute coronary syndromes (ACS), inflammation, and atherosclerosis. A range of molecules, present on the platelet surface and/or stored in platelet granules, contribute to the cross-talk of platelets with other inflammatory cells during the vascular inflammation involved in the development and progression of atherosclerosis. Platelets play a crucial role in plaque vulnerability. This chapter discusses the nature of these molecules and the mechanisms involved in the participation of platelets in atherosclerosis, with emphasis on vulnerable plaques and the role played by P-selectin, platelet-monocyte interactions, chemokines, and inflammatory cytokines.
