Key result
Targeting platelet GPVI and CLEC-2 receptors, along with their signaling tyrosine kinases, represents a promising novel strategy for treating thrombotic diseases with minimal disruption to hemostasis.
Why the study?
Current antiplatelet medications cause bleeding and recurrent thrombosis can still occur, highlighting the need for novel strategies targeting GPVI, CLEC-2, and tyrosine kinases that offer antithrombotic efficacy with minimal disruption to hemostasis.
Do novel antiplatelet strategies targeting GPVI, CLEC-2, and tyrosine kinases provide antithrombotic efficacy with minimal bleeding compared to conventional antiplatelet medications?
Do novel antiplatelet strategies targeting GPVI, CLEC-2, and tyrosine kinases provide antithrombotic efficacy with minimal bleeding compared to conventional antiplatelet medications?
Targeting GPVI, CLEC-2, and associated tyrosine kinases represents a promising novel antiplatelet strategy that may uncouple thrombosis prevention from bleeding risk.
Supports GPVI/CLEC-2 inhibitor development; leaves open whether these agents improve outcomes versus current antiplatelets in randomized trials.
Antiplatelet medications comprise the cornerstone of treatment for diseases that involve arterial thrombosis, including acute coronary syndromes (ACS), stroke and peripheral arterial disease. However, antiplatelet medications may cause bleeding and, furthermore, thrombotic events may still recur despite treatment. The interaction of collagen with GPVI receptors on the surface of platelets has been identified as one of the major players in the pathophysiology of arterial thrombosis that occurs following atherosclerotic plaque rupture. Promisingly, GPVI deficiency in humans appears to have a minimal impact on bleeding. These findings together suggest that targeting platelet GPVI may provide a novel treatment strategy that provides additional antithrombotic efficacy with minimal disruption of normal hemostasis compared to conventional antiplatelet medications. CLEC-2 is gaining interest as a therapeutic target for a variety of thrombo-inflammatory disorders including deep vein thrombosis (DVT) with treatment also predicted to cause minimal disruption to hemostasis. GPVI and CLEC-2 signal through Src, Syk and Tec family tyrosine kinases, providing additional strategies for inhibiting both receptors. In this review, we summarize the evidence regarding GPVI and CLEC-2 and strategies for inhibiting these receptors to inhibit platelet recruitment and activation in thrombotic diseases.
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Harbi et al. (2020) conducted a review in Thrombotic diseases. Inhibition of GPVI, CLEC-2 and tyrosine kinases was evaluated. Targeting platelet GPVI and CLEC-2 receptors, along with their signaling tyrosine kinases, represents a promising novel strategy for treating thrombotic diseases with minimal disruption to hemostasis.
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