AI Article Synopsis
- Platelet activation is key in stopping bleeding and can lead to blood clots, necessitating treatments that inhibit this process but carry bleeding risks.
- Current antithrombotic therapies are effective but risk bleeding, highlighting the need for safer alternatives.
- Targeting the platelet receptor GPVI shows promise as it can effectively reduce thrombosis and inflammation while maintaining normal blood clotting functions, paving the way for safer antiplatelet medications.
Article Abstract
Platelet activation is a crucial step in both physiological hemostasis and pathological thrombosis, which is an important mean to prevent and treat thrombotic diseases by inhibition of platelet activation. The current clinical antithrombotic therapy showed a high efficiency, but at risk of bleeding. Platelet glycoprotein VI (GPVI) is a platelet-specific receptor and its binding with collagen is critical for platelet activation. GPVI antagonists were shown to effectively inhibit thrombosis and inflammation without influence on normal hemostasis. As a novel target for antithrombotic therapy, it ideally combines efficacy with safety. This review summarizes the recent advances of studies on GPVI structure, function and its role in hemostasis, thrombosis, and anti-GPVI agents. The potential clinical strategies of antiplatelet drugs targeting GPVI are discussed so as to provide a reliable regimen for thrombotic diseases.
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| http://dx.doi.org/10.7534/j.issn.1009-2137.2017.01.048 | DOI Listing |
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