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Platelet adhesion receptors: novel targets for anti‐thrombotic therapy
Author(s) -
Williamson D.,
Giuliano S.,
Jackson S. P.
Publication year - 1999
Publication title -
australian and new zealand journal of medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.596
H-Index - 70
eISSN - 1445-5994
pISSN - 0004-8291
DOI - 10.1111/j.1445-5994.1999.tb00742.x
Subject(s) - platelet , platelet membrane glycoprotein , gpvi , von willebrand factor , medicine , platelet adhesiveness , receptor , adhesion , platelet activation , glycoprotein ib , microbiology and biotechnology , immunology , pharmacology , chemistry , biology , platelet aggregation , organic chemistry
The critical role of platelets in the development of the acute coronary syndromes is now well recognised, and a great deal of effort has therefore focused on elucidating the key adhesion receptors mediating platelet‐vessel wall and platelet‐platelet interactions. The vascular adhesion protein von Willebrand factor (vWf) plays a key role in supporting platelet adhesion to the damaged vessel wall and binds to two adhesion receptors on the platelet surface, the glycoprotein (GP) lb‐ V‐IX complex and glycoprotein IIb‐IIIa. The GP IIb‐V‐IX complex is a unique adhesion receptor which enables platelets to roll on a vWf matrix under conditions of rapid blood flow as well as transducing signals leading to the activation of GP IIb‐IIIa. This latter receptor binds to a distinct site on vWf and is essential for stabilising platelet adhesion to the site of vessel wall injury. In addition to supporting platelet adhesion, GP IIb‐IIIa plays a key role in a number of other platelet responses including platelet spreading, aggregation, the release of procoagulant‐rich microvesicles, and clot retraction. Given its central role in platelet function GP IIb‐IIIa has become an attractive target for the development of novel anti‐thrombotic agents. In this paper, we consider the advantages of inhibitors of GP IIb‐IIIa compared with other established anti‐platelet drugs including aspirin and ticlopidine, and also discuss some potential problems associated with the inhibition of GP IIb‐IIIa and other platelet adhesion receptors.