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there is an altered activation state of GPVI signaling in ST-elevation myocardial infarction patients; GPVI is critical for the formation of arterial thrombosis in vivo
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haplotype PEAN associated with SPS and manifested by fetal loss and suggest that the mechanism involved in the action of GPVI has significant effect on GPVI-mediated signal transduction through Syk-phosphorylation.
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This suggests whereas platelet receptor shedding is mainly modulated by calcium-dependent signals, either platelet-surface interactions with the container walls during storage or induced shear stress under long-term agitation, might be also involved in the excessive shedding of GPVI during the storage of PRP-platelet concentrates.
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There was no evidence to suggest that polymorphisms of GP VI T13254C and GP Ibalpha VNTR were associated with CAD.
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Platelet adhesion to collagen induces GPVI dimer clustering. GPVI clustering increases both avidity for collagen and the proximity of GPVI-associated signaling molecules, which may be crucial for the initiation and persistence of signaling
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Loss of the platelet surface receptors GPIbalpha and GPVI in heart failure, CF-VAD and ECMO patients may contribute to ablated platelet adhesion/activation, and limit thrombus formation under high/pathologic shear conditions
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SGPVI was significantly lower in patients treated with NOACs.
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Novel antithrombotic peptides derived from trowaglerix that acts through GPVI antagonism with greater safety-no severe bleeding.
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rs1613662 polymorphism has an important role in the development of venous thromboembolism in the white race
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plasma sGPVI levels are related to platelet activation in Living Donor Liver Transplantation. Although the plasma levels of sGPVI in the survivors increased after the operation, those in the nonsurvivors were high only on day 3.
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results support the idea that genetic variability of GP6 regulatory regions can be associated with platelet hyperaggregability - a possible cause of miscarriage
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These results demonstrate that GP6 is a receptor for fibrin and provide evidence that this interaction contributes to thrombus growth and stability.
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data suggest a novel role for FAK in GPVI-dependent ROS formation and platelet activation and elucidate a proximal signaling role for FAK within the GPVI pathway.
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As sCD147 strongly correlates with platelet-specific sGPVI, a common platelet source and/or mechanism of release may contribute to sCD147 levels in vivo.
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This study identifies GPVI as a platelet receptor for polymerized fibrin with 2 major functions: (1) amplification of thrombin generation and (2) recruitment of circulating platelets to clots.
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measuring the level of sGPVI may be useful for assessing the activation of platelets in postoperative patients treated with anti-Xa agents and also for predicting the incidence of VTE in this population.
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Glaucocalyxin A inhibits platelet activation and thrombus formation preferentially via GPVI signaling pathway.
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The plasma levels of sGPVI were the highest in patients with TMA without markedly reduced ADAMTS13 and those were significantly reduced after plasma exchange.
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Results suggest that variants of GP6 SNPs, namely, rs1671153, rs1654410, rs1654419, and rs1613662, may be associated with risk of recurrent miscarriage.
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Lower platelet GPIV levels are associated with no-reflow phenomenon in patients with acute myocardial infarction.
