ArticlePloS one2022
Platelet surface receptor glycoprotein VI-dimer is overexpressed in stroke: The Glycoprotein VI in Stroke (GYPSIE) study results.
Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Serum GPVI for Diagnostic Assessment and Short-Term Risk Stratification in Patients with Suspected Transient Ischemic Attack: A Prospective Observational Cohort Study.Brain sciences · 2026Article
- Research advances on platelet glycoprotein VI in ischemic stroke.Thrombosis journal · 2026Review
- Role of glycoproteins in hepatic lipid metabolism: emerging diagnostic markers and therapeutic targets.PeerJ · 2025Review
- Targeting Rap1b signaling cascades with CDNF: Mitigating platelet activation, plasma oxylipins and reperfusion injury in stroke.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Mendelian Randomization and Bayesian Colocalization Analysis Implicate Glycoprotein VI as a Potential Drug Target for Cardioembolic Stroke in South Asian Populations.Journal of the American Heart Association · 2024Article
- Affimer reagents as tool molecules to modulate platelet GPVI-ligand interactions and specifically bind GPVI dimer.Blood advances · 2024Article
- Immunothrombosis in neurovascular disease.Research and practice in thrombosis and haemostasis · 2024Article
- Platelet Receptor Glycoprotein VI-Dimer Is Overexpressed in Patients with Atrial Fibrillation at High Risk of Ischemic Stroke.TH open : companion journal to thrombosis and haemostasis · 2023Article
- Coagulation biomarkers for ischemic stroke.Research and practice in thrombosis and haemostasis · 2023Article
- Organ and cell-specific biomarkers of Long-COVID identified with targeted proteomics and machine learning.Molecular medicine (Cambridge, Mass.) · 2023Article
- Should aspirin be replaced with ADP blockers and anti-GPVI to manage thrombosis?Vascular biology (Bristol, England) · 2023Review
- Thrombo-Inflammation and Immunological Response in Ischemic Stroke: Focusing on Platelet-Tregs Interaction.Frontiers in cellular neuroscience · 2022Review
- Perspective: Collagen induced platelet activationFrontiers in cardiovascular medicine · 2022Article
- Improving treatment for acute ischemic stroke-Clot busting innovation in the pipeline.Frontiers in medical technology · 2022Article
- C1-inhibitor influence on platelet activation by thrombin receptors agonists.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisArticle
Corrections and comments
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Authors and funding
18 authors at 2 institutions in 2 countries.
Funding
Abstract
objectivesPlatelet activation underpins thrombus formation in ischemic stroke. The active, dimeric form of platelet receptor glycoprotein (GP) VI plays key roles by binding platelet ligands collagen and fibrin, leading to platelet activation. We investigated whether patients presenting with stroke expressed more GPVI on their platelet surface and had more active circulating platelets as measured by platelet P-selectin exposure.
methods129 ischemic or hemorrhagic stroke patients were recruited within 8h of symptom onset. Whole blood was analyzed for platelet-surface expression of total GPVI, GPVI-dimer, and P-selectin by flow cytometry at admission and day-90 post-stroke. Results were compared against a healthy control population (n = 301).
resultsThe platelets of stroke patients expressed significantly higher total GPVI and GPVI-dimer (P<0.0001) as well as demonstrating higher resting P-selectin exposure (P<0.0001), a measure of platelet activity, compared to the control group, suggesting increased circulating platelet activation. GPVI-dimer expression was strongly correlated circulating platelet activation [r2 = 0.88, P<0.0001] in stroke patients. Furthermore, higher platelet surface GPVI expression was associated with increased stroke severity at admission. At day-90 post-stroke, GPVI-dimer expression and was further raised compared to the level at admission (P<0.0001) despite anti-thrombotic therapy. All ischemic stroke subtypes and hemorrhagic strokes expressed significantly higher GPVI-dimer compared to controls (P<0.0001).
conclusionsStroke patients express more GPVI-dimer on their platelet surface at presentation, lasting at least until day-90 post-stroke. Small molecule GPVI-dimer inhibitors are currently in development and the results of this study validate that GPVI-dimer as an anti-thrombotic target in ischemic stroke.
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