Formation of the clot.

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.

• Authors: Bruce Furie, Barbara C Furie
• Journal: Thrombosis research (Thromb Res) Vol. 130 Suppl 1 Pg. S44-6 (Oct 2012) ISSN: 1879-2472 [Electronic] United States
• PMID: 23026660 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Review)
• Copyright: Copyright © 2012 Elsevier Ltd. All rights reserved.

Chemical References

• Enzyme Inhibitors
• Fibrinolytic Agents
• Platelet Aggregation Inhibitors
• Fibrin
• Thrombin
• Protein Disulfide-Isomerases

Topics

• Animals
• Blood Platelets (drug effects, enzymology)
• Drug Design
• Enzyme Inhibitors (pharmacology)
• Fibrin (metabolism)
• Fibrinolytic Agents (pharmacology)
• Humans
• Kinetics
• Microscopy, Confocal
• Microscopy, Video
• Platelet Aggregation
• Platelet Aggregation Inhibitors (pharmacology)
• Protein Disulfide-Isomerases (antagonists & inhibitors, blood)
• Thrombin (metabolism)
• Thrombosis (blood, drug therapy, enzymology)