Is thrombin the problem or (dis)solution?

摘要

Platelet thrombus formation is a dynamic process that is essential for the cessation of bleeding at sites of vascular injury. Dys- regulation of this process can lead to excessive thrombus formation, particularly at sites of atherosclerotic plaque rupture, precipitating the acute coronary syndromes or ischemic stroke. The hemostatic response is regulated by competing prothrombotic and antithrom-botic forces. A key player in this regard is the serine protease, thrombin.' In its free form, thrombin is procoagulant, activating several components of the coagulation cascade as well as converting fibrinogen to fibrin. It is also one of the most potent platelet agonists known. Conversely, thrombin bound to thrombo-modulin on vascular endothelial cells can activate protein C, a potent physiologic anticoagulant.