Novel mechanisms of platelet activation and sustained signalling through GPVI and PAR1

Upon vascular injury, platelets interact with exposed ligands, whereafter they become activated and form a platelet plug, to minimize blood loss. However, unwanted platelet activation can lead to arterial thrombosis, hart infarcts and stroke. There is still an unmet clinical need for the development of novel antiplatelet drugs, which inhibit thrombosis, without increasing the bleeding risk. This thesis investigated acute and persistent mechanisms of platelet activation, mainly via the platelet receptors GPVI and PAR1, which are interesting and potential targets for novel antiplatelet therapy. The novel insights into the mechanisms involved in platelet activation via GPVI and PAR1 contribute to a better understanding of the complex platelet activation mechanisms in thrombosis and haemostasis.