Platelet coagulation-protein interactions.
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.
Walsh
Peter N
PN
The Sol Sherry Thrombosis Research Center, The Sol Sherry Thrombosis Research Center, Department of Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA. pnw@temple.edu
D001777:Blood Coagulation / Q000502:physiology*; D001778:Blood Coagulation Disorders; D001779:Blood Coagulation Factors / Q000235:genetics / Q000502:physiology*; D001792:Blood Platelets / Q000502:physiology*; D006487:Hemostasis; D006801:Humans; D013925:Thromboplastin / Q000502:physiology; D013927:Thrombosis / Q000097:blood / Q000517:prevention & control
D001779:Blood Coagulation Factors; D013925:Thromboplastin