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Abstract
Platelets, the smallest blood cells play a central role in the process of hemostasis and thrombosis. This central role is carried through integrated steps of platelet activation, adhesion, secretion and aggregation.
Platelet activation is inhibited during normal arterial flow by intact endothelium that releases antithrombogenic factors, however when vascular endothelium is injured, platelets are activated through various mediators like collagen and ADP leading to subsequent platelet activity.
Platelet adhesion is carried through initial binding of platelet receptor GPIb-V-IX to its agonist vWF followed by binding GPVI receptor to subendothelial collagen, the step that provide stable platelet adhesion, promote platelet secretion and aggregation.
Platelet secretion results in the release of several granule components which modulates functions of interacting platelets and other cells.
Platelet aggregation is carried through binding of fibrinogen to its specific receptor GPIIb/IIIa forming fibrinogen bridges between platelets that result in firm connection stabilizing platelet aggregate.
Many genetic polymorphisms were found to be affecting normal platelet function either by affecting quantity or quality of the protein product produced by the polymorphic gene.