ArticleNature communications2024
Platelet integrin αIIbβ3 plays a key role in a venous thrombogenesis mouse model.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Shared ligand-blocking mechanism but distinct conformational modulation by α5-targeting antibodies BIIG2 and MINT1526A.Structure (London, England : 1993) · 2026Article
- Harnessing flavonoids as innovative agents for the modulation of platelet activation and thrombotic disorders.Molecular biology reports · 2026Review
- Tanyu Tongzhi Decoction Improves Cardiac Function by Inhibiting Platelet Activation and Alleviating Coronary Microthrombosis for Coronary Heart Disease Mice.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Advances in native cell membrane nanoparticles system.Current opinion in structural biology · 2025Review
- Venous thrombosis unchained: Pandora's box of noninflammatory mechanisms.Blood advances · 2025Review
- Advancing Platelet Research Through Live-Cell Imaging: Challenges, Techniques, and Insights.Sensors (Basel, Switzerland) · 2025Review
- The Integrin Receptors: From Discovery to Structure to Medicines.Immunological reviews · 2025Review
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15 authors.
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Abstract
Venous thrombosis (VT) is a common vascular disease associated with reduced survival and a high recurrence rate. VT is initiated by the accumulation of platelets and neutrophils at sites of endothelial cell activation. A role for platelet αIIbβ3 in VT is not established, a task complicated by the increased bleeding risk caused by partial agonists such as tirofiban. Here, we show that m-tirofiban, a modified version of tirofiban, does not agonize αIIbβ3 based on lack of neoepitope expression and the cryo-EM structure of m-tirofiban/full-length αIIbβ3 complex. m-tirofiban abolishes agonist-induced platelet aggregation while preserving clot retraction ex vivo and, unlike tirofiban, it suppresses venous thrombogenesis in a mouse model without increasing bleeding. These findings establish a key role for αIIbβ3 in VT initiation and suggest that m-tirofiban and compounds with a similar structurally-defined mechanism of action merit consideration as potential thromboprophylaxis agents in patients at high risk for VT and hemorrhage.
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