Abstract
An electron transport system regulates the initiation of thrombus formation through the activation of critical receptors involved in hemostasis and thrombosis. Protein disulfide isomerase along with other thiol isomerases, important for intracellular protein synthesis, are responsible for this extracellular activity during thrombus formation. Inhibition of these thiol isomerases blocks platelet aggregation and fibrin generation. Pharmaceuticals directed against these thiol isomerases offers a novel approach to antithrombotic therapy.