This review outlines the 'two-site, two-step' model of platelet-collagen interactions, providing mechanistic insights into normal hemostasis and pathological thrombosis.
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Refines platelet-collagen interaction models in thrombosis; leaves open targeted therapy development pending clinical validation.
Platelet adhesion to and activation by exposed subendothelial collagen plays a critical role in normal haemostasis and pathological thrombosis. Recent advances in elucidating the mechanisms underlying platelet-collagen interaction support a 'two-site, two-step' model. Direct platelet binding to integrin alpha2beta1 mainly sustains adhesion and allows recognition of glycoprotein VI. The latter interaction is responsible for characteristic intracellular signalling events leading to p72Syk and PLCgamma2 activation. The present review describes the known collagen receptors on platelets and discusses the current understanding of signal transduction promoted by collagen.
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Alberio et al. (1999) studied this question.
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