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GPVI targeting may enable safer antithrombotics; leaves open confirmation of clinical bleeding benefit in trials.
a l i t y a n d m o r b i d i t y w o r l d w i d e . Al t h o u g h t h e r e c e n t advancements in existing anti-platelet therapeutics have significantly reduced the burden of cardiovascular deaths but owing to their global impact on primary haemostasis, their clinical benefits are often limited by bleeding risk. Recent developments in the understanding of platelet biology have placed platelet-collagen interaction at the critical position in the sequence of events during arterial thrombosis. Thus there is considerable interest in developing novel therapeutic strategies against platelet collagen receptor glycoprotein VI (GPVI) because not only its selective blockade or deficiency holds promise for the reduced risk of bleeding complications as evidenced in mice and humans, but also the exclusive expression of GPVI on platelets and megakaryocytes offers to prevent the adverse off-target effects of antithrombotic drugs. The present review summarizes recent developments in understanding of platelet functions during arterial thrombosis and structural and functional attributes of platelet GPVI to identify it as a novel antithrombotic drug target. Moreover, it
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Misra et al. (2014) studied this question.
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