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Semin Thromb Hemost 2004; 30(4): 461-471
DOI: 10.1055/s-2004-833481
DOI: 10.1055/s-2004-833481
Platelet Coagulation-Protein Interactions
Further Information
Publication History
Publication Date:
08 September 2004 (online)
The biochemical mechanisms by which activated platelets participate in exposing receptors for the assembly of enzyme-cofactor-substrate complexes at all stages of the blood coagulation cascade are reviewed. Information derived from studies conducted during the last 30 years supports the concept that the initiation of blood coagulation is triggered by exposure of tissue factor at injury sites, leading to the generation of minute quantities of thrombin (limited by tissue factor pathway inhibitor), sufficient to activate platelets, factors XI, VIII, and V, and trigger the consolidation pathway (i.e., the sequential activation of factors XI, IX, X, and prothrombin on the activated platelet surface), leading to the generation of sufficient thrombin to convert fibrinogen to fibrin and effect hemostasis. Platelets localize coagulation to the hemostatic thrombus and protect coagulation enzymes from inhibition by both plasma and platelet inhibitors (e.g., protease nexin 2), thus preventing disseminated intravascular coagulation.
KEYWORDS
Consolidation pathway of coagulation - tissue factor pathway of coagulation - platelet receptors for coagulation proteins
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Professor
Peter N WalshM.D. Ph.D.
Sol Sherry Thrombosis Research Center, Temple University School of Medicine
3400 North Broad Street
Philadelphia, PA 19140
Email: pnw@temple.edu