Abstract

Platelets play a key role in arterial thrombosis, a frequent and life-threatening condition. Upon vascular injury, platelets are rapidly recruited to the site of endothelial disruption, where they become activated and critically contribute to the formation of an occlusive clot. To treat or prevent arterial thrombosis, various antiplatelet therapies have been developed. However, many pathways targeted are also involved in hemostasis. Their inhibition therefore poses an increased risk of bleeding. To date it remains an eminent task to identify thrombosis-specific pathways in arterial thrombosis. Platelet receptors and intracellular molecules, whose absence does not cause overt bleeding in humans, may open up new therapeutic avenues. We here recapitulate the pathophysiology of arterial thrombosis and present newly identified pathways, which may serve as drug targets in the future. Finally, we will discuss the reciprocal interactions of platelets and innate immune cells and their potential role in arterial thrombosis. A detailed understanding of the mechanisms underlying this life-threatening condition is crucial for future research and the development of novel therapies.

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