ReviewJRSM cardiovascular disease2012
The platelet fibrinogen receptor: from megakaryocyte to the mortuary.
Review in JRSM cardiovascular disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 3 syntheses or guidelines pooled it, 42 citations in OpenAlex.
- The PlA1/A2 polymorphism of glycoprotein IIIa in relation to efficacy of antiplatelet drugs: a systematic review and meta-analysis.British journal of clinical pharmacology · 2014Pooled it
- The PlA1/A2 polymorphism of glycoprotein IIIa as a risk factor for stroke: a systematic review and meta-analysis.PloS one · 2014Pooled it
- The PlA1/A2 polymorphism of glycoprotein IIIa as a risk factor for myocardial infarction: a meta-analysis.PloS one · 2014Pooled it
- Fibrinogen-Drug Nanoparticles Achieve Durable Responses in Pancreatic and Breast Cancer Murine Models.ACS pharmacology & translational science · 2026Article
- Epidemiological and clinical characteristics of children and young adults with Glanzmann's thrombasthenia in upper Egypt: a multicenter cross-sectional study.Annals of hematology · 2025Observational
- Shedding Light on the Cell Biology of Platelet-Derived Extracellular Vesicles and Their Biomedical Applications.Life (Basel, Switzerland) · 2023Review
- An Insight into Recent Advances on Platelet Function in Health and Disease.International journal of molecular sciences · 2022Review
- MicroRNA 320a and Membrane Antigens as Tools to Evaluate the Pathophysiology of Platelets Stored in Blood Banks.Current issues in molecular biology · 2022Article
- The effects of estrogen and hormone replacement therapy on platelet activity: a review.American journal of blood research · 2022Review
- Matching the Cellulose/Silica Films Surface Properties for Design of Biomaterials That Modulate Extracellular Matrix.Membranes · 2021Article
- Microfluidic chip grafted with integrin tension sensors for evaluating the effects of flowing shear stress and ROCK inhibitor on platelets.Lab on a chip · 2021Article
- Molybdenum derived from nanomaterials incorporates into molybdenum enzymes and affects their activities in vivo.Nature nanotechnology · 2021Article
- Evaluation of Blood Coagulation Parameters and ADMA, NO, IL-6, and IL-18 Serum Levels in Patients with Neovascular AMD before, during, and after the Initial Loading Phase of Intravitreal Aflibercept.Life (Basel, Switzerland) · 2021Article
- Runx1 promotes scar deposition and inhibits myocardial proliferation and survival during zebrafish heart regeneration.Development (Cambridge, England) · 2020Article
- Unexpected low expression of platelet fibrinogen receptor in patients with chronic myeloproliferative neoplasms: how does it change with aspirin?British journal of haematology · 2020Article
- The TXA2R rs1131882, P2Y1 rs1371097 and GPIIIa rs2317676 three-loci interactions may increase the risk of carotid stenosis in patients with ischemic stroke.BMC neurology · 2019Article
- Interactions among variants inOncotarget · 2018Article
- Interaction amongOncotarget · 2017Article
- Opposite effects ofAnnals of translational medicine · 2017Article
- Platelet receptor Gene (P2Y12, P2Y1) and platelet glycoprotein Gene (GPIIIa) polymorphisms are associated with antiplatelet drug responsiveness and clinical outcomes after acute minor ischemic stroke.European journal of clinical pharmacology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Platelets are integral to normal haemostatic function and act to control vascular haemorrhage with the formation of a stable clot. The fibrinogen receptor (glycoprotein IIb/IIIa [GPIIb/IIIa]) is the most abundant platelet integrin and, by binding fibrinogen, facilitates irreversible binding of platelets to the exposed extracellular matrix and enables the cross-linking of adjacent platelets. The vital role of GPIIb/IIIa requires tight control of both its synthesis and function. After transcription from distinct domains on chromosome 17, the two subunits of the heterodimer are carefully directed through organelles with intricate regulatory steps designed to prevent the cellular expression of a dysfunctional receptor. Similarly, exquisite control of platelet activation via bidirectional signalling acts to limit the inappropriate and excessive formation of platelet-mediated thrombus. However, the enormous diversity of genetic mutations in the fibrinogen receptor has resulted in a number of allelic variants becoming established. The Pro(33) polymorphism in GPIIIa is associated with increased cardiovascular risk due to a pathological persistence of outside-in signalling once fibrinogen has dissociated from the receptor. The polymorphism has also been associated with the phenomenon of aspirin resistance, although larger epidemiological studies are required to establish this conclusively. A failure of appropriate receptor function due to a diverse range of mutations in both structural and signalling domains, results in the bleeding diathesis Glanzmann's thrombasthaenia. GPIIb/IIIa inhibitors were the first rationally designed anti-platelet drugs and have proven to be a successful therapeutic option in high-risk primary coronary intervention. As our understanding of bidirectional signalling improves, more subtle and directed therapeutic strategies may be developed.
Identifiers
What OpenQuestion holds
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.