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Updated: Jan 23, 2026

A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry
Published on: June 5, 2019
Blood platelet surface receptor genetic variation and risk of thrombotic episodes
Rafal Szelenberger1, Michal Kacprzak2, Michal Bijak1
1Department of General Biochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Pomorska 141/143, 90-236 Lodz, Poland.
Haemostasis is a set of processes whose main task is to prevent blood loss by creating barriers in damaged vessels. Because of the large number of platelet surface receptors and their many agonists, platelets can be activated in normal and pathologic states leading to thromboembolic complications. Although age, blood pressure, LDL and HDL, diabetes, lack of physical activity, obesity and stress are well established risk factors, recent work has shown that platelet receptor polymorphisms also impact platelet function. The most common polymorphisms include 14A/T (PAR-1), 139C/T, 744T/C, 52G/T, i-ins801A (P2Y12), 1622A/G, -5T/C (GPIbα) 1565C/T (GPIIb/IIIa) and 807C/T (GPIa/IIa). This review examines the influence of these polymorphisms on cardiovascular disease including myocardial infarction, deep venous thromboembolism and acute coronary syndromes. Elucidation of these genetic variations will facilitate our understanding of the complex molecular mechanisms involved with physiologic and pathophysiologic platelet activation and clot formation.
Haemostasis is a set of processes whose main task is to prevent blood loss by creating barriers in damaged vessels. Because of the large number of platelet surface receptors and their many agonists, platelets can be activated in normal and pathologic states leading to thromboembolic complications. Although age, blood pressure, LDL and HDL, diabetes, lack of physical activity, obesity and stress are well established risk factors, recent work has shown that platelet receptor polymorphisms also impact platelet function. The most common polymorphisms include 14A/T (PAR-1), 139C/T, 744T/C, 52G/T, i-ins801A (P2Y12), 1622A/G, -5T/C (GPIbα) 1565C/T (GPIIb/IIIa) and 807C/T (GPIa/IIa). This review examines the influence of these polymorphisms on cardiovascular disease including myocardial infarction, deep venous thromboembolism and acute coronary syndromes. Elucidation of these genetic variations will facilitate our understanding of the complex molecular mechanisms involved with physiologic and pathophysiologic platelet activation and clot formation.
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