ReviewInternational journal of molecular sciences2022
Reversible Platelet Integrin αIIbβ3 Activation and Thrombus Instability.
Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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
30 citing papers in PubMed, 37 citations in OpenAlex.
- Selective inhibition of platelet inflammatory tether formation via force-modulated vibrational states of integrin αIIbβ3.Journal of molecular modeling · 2026Article
- Surface cues shape procoagulant properties of amyloidogenic microclots.Cell death & disease · 2026Review
- Platelet CLEC-2 activation leads to GPIb⍺ shedding: Implications for doxorubicin chemotherapy and thrombosis.The Journal of biological chemistry · 2026Article
- When GPVI Goes Rogue: Pathogenesis and Therapeutic Horizons in ITP.Expert reviews in molecular medicine · 2026Review
- Aβ₁₋₄₀ Enhances Platelet Sensitivity to Thrombin via NADPH Oxidase-ROS Signaling and Integrin αBiomolecules & therapeutics · 2026Article
- Levels of Talin1 in Platelet-Derived Microvesicles Affect Platelet Activation in Patients with Nonvalvular Atrial Fibrillation.Biochemical genetics · 2026Article
- Exploring Molecular Mechanism of Thymoquinone via cMet and PDGFR for Accelerated Hemostasis: An Approach Through In Silico, In Vitro, and In Vivo Studies.Chemistry & biodiversity · 2026Article
- Fibrin Monomer in Thrombosis and Haemostasis: A Clinical Biomarker and Beyond.International journal of molecular sciences · 2025Review
- Article
- Characterization of Novel Variants inBiomolecules · 2025Article
- The Multifaceted Role of Platelets in Atherosclerosis and Ischemic Disease: Pathogenesis, Inflammation, and Therapeutic Opportunities.Life (Basel, Switzerland) · 2025Review
- Dihydrogeodin fromMarine drugs · 2025Article
- Platelets and diseases: signal transduction and advances in targeted therapy.Signal transduction and targeted therapy · 2025Review
- Article
- ZO-2 seals the deal for platelet tight junctions.Research and practice in thrombosis and haemostasis · 2025Article
- 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
- Conformational response of αStructure (London, England : 1993) · 2025Article
- The Reactive Oxygen Species Scavenger N-Acetyl-L-Cysteine Reduces Storage-Dependent Decline in IntegrinOxidative medicine and cellular longevity · 2025Article
- Emerging Elastic Micro-Nano Materials for Diagnosis and Treatment of Thrombosis.Research (Washington, D.C.) · 2025Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Integrin αIIbβ3 activation is essential for platelet aggregation and, accordingly, for hemostasis and arterial thrombosis. The αIIbβ3 integrin is highly expressed on platelets and requires an activation step for binding to fibrinogen, fibrin or von Willebrand factor (VWF). A current model assumes that the process of integrin activation relies on actomyosin force-dependent molecular changes from a bent-closed and extended-closed to an extended-open conformation. In this paper we review the pathways that point to a functional reversibility of platelet αIIbβ3 activation and transient aggregation. Furthermore, we refer to mouse models indicating that genetic defects that lead to reversible platelet aggregation can also cause instable thrombus formation. We discuss the platelet agonists and signaling pathways that lead to a transient binding of ligands to integrin αIIbβ3. Our analysis points to the (autocrine) ADP P2Y
Indexed as
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.