Molecular regulation of platelet-dependent thrombosis.
Hemostasis is a normal process preventing the sequelae of uncontrolled hemorrhage. In certain settings, these same processes cause adverse clinical events due to thrombotic occlusion of a vessel. The majority of unstable coronary syndromes result from disruption of an atherosclerotic plaque, leading to the exposure of subintimal contents, which triggers coagulation and the formation of a platelet-rich thrombus. The central role of platelet activation in the events that lead to vessel occlusion is well known. However, this process is complex and influenced by a myriad of cellular and plasma-derived mediators that regulate the balance between occlusive and nonocclusive thrombosis.
Freedman
Jane E
JE
Boston University School of Medicine, Whitaker Cardiovascular Institute, Boston, MA 02118, USA. freedmaj@bu.edu
D001792:Blood Platelets / Q000502:physiology*; D006801:Humans; D010973:Platelet Adhesiveness / Q000502:physiology*; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D013927:Thrombosis / Q000097:blood* / Q000517:prevention & control; D014841:von Willebrand Factor / Q000502:physiology
D010975:Platelet Aggregation Inhibitors; D014841:von Willebrand Factor