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(Circulation. 2005;112:2725-2734.)
© 2005 American Heart Association, Inc.

Basic Science for Clinicians

Molecular Regulation of Platelet-Dependent Thrombosis

Jane E. Freedman, MD

From the Boston University School of Medicine, Whitaker Cardiovascular Institute, Boston, Mass.

Correspondence to Jane E. Freedman, MD, Boston University School of Medicine, Whitaker Cardiovascular Institute, 715 Albany St, W507, Boston, MA 02118. E-mail freedmaj{at}bu.edu

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.

Key Words: coagulation • platelets • thrombosis

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