Getting a GRP on tissue factor activation.

Atherothrombosis, defined as atherosclerotic lesion disruption with superimposed thrombosis, is the underlying cause of cardiovascular disease that accounts for the majority of deaths in North America.1 Thrombosis at these sites is triggered by tissue factor (TF), an integral membrane glycoprotein essential for the initiation of blood coagulation.2 TF-dependent procoagulant activity occurs on the surface of cells and is induced by a wide range of physiological agents/conditions, including endotoxin,3 viral infection,4 hypoxia,5 apoptosis,6 homocysteine,7 and reactive oxygen species.8 Furthermore, tumor cells express TF and the prothrombotic state observed in cancer patients has been largely attributed to increased TF procoagulant activity.9 Thus, the ability to inhibit TF-dependent procoagulant activity after plaque disruption would likely alleviate many of the acute clinical manifestations of cardiovascular disease.