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Glycoprotein IIb/IIIa in Platelet Aggregation and Acute Arterial Thrombosis

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Part of the book series: Contemporary Cardiology ((CONCARD))

Abstract

Glycoprotein (GP) IIb/IIIa antagonists have been shown to therapeutically regulate platelet function to prevent, for example, the thrombotic complications associated with coronary artery disease (1). Moreover, it is now suggested that the modulation of GPIIb/IIIa affects not only platelet aggregation and thrombosis, but also inflammation, which might ultimately result in a reduction of recurrent thrombotic events. Three main reasons explain why GPIIb/IIIa (αIIb β3 integrin) (2) is an ideal platelet target for the treatment of acute -IIbbarterial thrombosis and why the development of GPIIb/IIIa antagonists has been successful. First, GPIIb/IIIa is on the “final common pathway” (3) mediating platelet aggregation, a process central to acute arterial thrombosis, irrespective of the agonist used to induce platelet activation. Second, GPIIb/IIIa is a platelet-specific glycoprotein, the most abundant protein on the platelet surface. Third, the dynamic nature of GPIIb/IIIa allows it to affect a variety of platelet responses, therefore allowing GPIIb/IIIa antagonists to modulate a variety of platelet functions including those involved in coagulation, inflammation, fibrinolysis, and vascular cell proliferation.

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Andre, P., Phillips, D.R. (2003). Glycoprotein IIb/IIIa in Platelet Aggregation and Acute Arterial Thrombosis. In: Lincoff, A.M. (eds) Platelet Glycoprotein IIb/IIIa Inhibitors in Cardiovascular Disease. Contemporary Cardiology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-376-7_3

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