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- W3111917059 endingPage "41" @default.
- W3111917059 startingPage "29" @default.
- W3111917059 abstract "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." @default.
- W3111917059 created "2020-12-21" @default.
- W3111917059 creator A5032131277 @default.
- W3111917059 creator A5043982558 @default.
- W3111917059 creator A5057799772 @default.
- W3111917059 creator A5064200055 @default.
- W3111917059 creator A5067098592 @default.
- W3111917059 date "2020-12-13" @default.
- W3111917059 modified "2023-10-16" @default.
- W3111917059 title "Novel antiplatelet strategies targeting GPVI, CLEC-2 and tyrosine kinases" @default.
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