ArticleBlood2015
Fibrin activates GPVI in human and mouse platelets.
Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
104 citing papers in PubMed, 254 citations in OpenAlex.
- Soluble CLEC-2 as an Emerging Biomarker of In Vivo Platelet Activation.Journal of clinical medicine · 2026Review
- Procoagulant platelets: linking coagulation and thromboinflammation in cardiovascular disease.Nature reviews. Cardiology · 2026Review
- Costunolide, a Sesquiterpene Lactone, Protects Against Platelet Activation and Thrombus Formation.Cells · 2026Article
- The journey of maternal platelets through the utero-placental circulation: routes, interactions, and physiological implications.Molecular human reproduction · 2026Review
- Research advances on platelet glycoprotein VI in ischemic stroke.Thrombosis journal · 2026Review
- Platelet effector functions in inflammation.Research and practice in thrombosis and haemostasis · 2026Review
- Platelet Membrane Receptors and Signalling Pathways.Handbook of experimental pharmacology · 2026Review
- Fibrin Monomer in Thrombosis and Haemostasis: A Clinical Biomarker and Beyond.International journal of molecular sciences · 2025Review
- Newcastle disease virus acquires phosphatidylserine through the budding process to enhance infectivity.Virulence · 2025Article
- Humanized murine models of platelet function.Current opinion in hematology · 2025Review
- Biomechanical platelet activation: diseases that require a new class of antiplatelet therapeutics.American journal of physiology. Cell physiology · 2025Review
- A Novel KGD-Based αIIbβ3 Antagonist Prevents Arterial Thrombosis While Preserving Hemostasis and Avoiding Thrombocytopenia.International journal of molecular sciences · 2025Article
- Oxygen Concentration Plays a Critical Role in Fibrinogen-Mediated Platelet Activation via Inactivation of αBiomolecules · 2025Article
- Fragmented thrombi, targeted solutions: Exploring GPVI inhibition in high-shear environments.Biophysical journal · 2025Article
- A naphthalimide derivative exerts potent antiplatelet and antithrombotic activities without a bleeding tendency.Frontiers in pharmacology · 2025Article
- Neuroinflammation and acute ischemic stroke: impact on translational research and clinical care.Frontiers in surgery · 2025Review
- Post-translational modifications of fibrinogen: implications for clotting, fibrin structure and degradation.Molecular biomedicine · 2024Review
- Soluble glycoprotein VI predicts abdominal aortic aneurysm growth rate and is a novel therapeutic target.Blood · 2024Article
- Beyond basic characterization and omics: Immunomodulatory roles of platelet-derived extracellular vesicles unveiled by functional testing.Journal of extracellular vesicles · 2024Article
- Functional characterization of a nanobody-based glycoprotein VI-specific platelet agonist.Research and practice in thrombosis and haemostasis · 2024Article
44 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The glycoprotein VI (GPVI)-Fc receptor γ (FcRγ) chain is the major platelet signaling receptor for collagen. Paradoxically, in a FeCl3 injury model, occlusion, but not initiation of thrombus formation, is delayed in GPVI-deficient and GPVI-depleted mice. In this study, we demonstrate that GPVI is a receptor for fibrin and speculate that this contributes to development of an occlusive thrombus. We observed a marked increase in tyrosine phosphorylation, including the FcRγ chain and Syk, in human and mouse platelets induced by thrombin in the presence of fibrinogen and the αIIbβ3 blocker eptifibatide. This was not seen in platelets stimulated by a protease activated receptor (PAR)-4 peptide, which is unable to generate fibrin from fibrinogen. The pattern of tyrosine phosphorylation was similar to that induced by activation of GPVI. Consistent with this, thrombin did not induce tyrosine phosphorylation of Syk and the FcRγ chain in GPVI-deficient mouse platelets. Mouse platelets underwent full spreading on fibrin but not fibrinogen, which was blocked in the presence of a Src kinase inhibitor or in the absence of GPVI. Spreading on fibrin was associated with phosphatidylserine exposure (procoagulant activity), and this too was blocked in GPVI-deficient platelets. The ectodomain of GPVI was shown to bind to immobilized monomeric and polymerized fibrin. A marked increase in embolization was seen following FeCl3 injury in GPVI-deficient mice, likely contributing to the delay in occlusion in this model. These results demonstrate that GPVI is a receptor for fibrin and provide evidence that this interaction contributes to thrombus growth and stability.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.