ArticleJournal of thrombosis and haemostasis : JTH2020
Model-dependent contributions of FXII and FXI to venous thrombosis in mice.
Article in Journal of thrombosis and haemostasis : JTH, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Emerging strategies in venous thromboembolism: a narrative review of pharmacological innovations.Thrombosis journal · 2026Review
- Targeting factor XI for venous thromboembolism prevention: a tale of 2 antibodies.Journal of thrombosis and haemostasis : JTH · 2026Article
- MiR-582-3p regulates endothelial cell function in lower extremity deep vein thrombosis by targeting TFRC.Annals of hematology · 2026Article
- Hypoxia-inducible factors contribute to venous thrombosis in a mouse model of myeloproliferative neoplasms.Blood advances · 2026Article
- Plasminogen activation and plasmin activity are not necessary to prevent venous thrombosis/thromboembolism.Blood · 2025Observational
- Coagulation factor XII haploinsufficiency is protective against venous thromboembolism in a population-scale multidimensional analysis.Nature communications · 2025Article
- Factor XII-driven coagulation traps bacterial infections.The Journal of experimental medicine · 2025Article
- Addressing the pathophysiology of venous thrombosis and chronic kidney disease in sickle cell trait using a mouse model.Blood advances · 2025Article
- Article
- Factor XI localization in human deep venous thrombus and function of activated factor XI on venous thrombus formation and hemostasis.Research and practice in thrombosis and haemostasis · 2025Article
- Plasma kallikrein supports FXII-independent thrombin generation in mouse whole blood.Blood advances · 2024Article
- Cutting-Edge Techniques and Drugs for the Treatment of Pulmonary Embolism: Current Knowledge and Future Perspectives.Journal of clinical medicine · 2024Review
- High plasma levels of C1-inhibitor are associated with lower risk of future venous thromboembolism.Journal of thrombosis and haemostasis : JTH · 2023Article
- C1 inhibitor deficiency enhances contact pathway-mediated activation of coagulation and venous thrombosis.Blood · 2023Article
- Factor XII contributes to thrombotic complications and vaso-occlusion in sickle cell disease.Blood · 2023Article
- Underlying mechanisms of thrombus formation/growth in atherothrombosis and deep vein thrombosis.Pathology international · 2023Review
- Neutrophil extracellular traps mediate deep vein thrombosis: from mechanism to therapy.Frontiers in immunology · 2023Review
- Genetic deletion of platelet PAR4 results in reduced thrombosis and impaired hemostatic plug stability.Journal of thrombosis and haemostasis : JTH · 2022Article
- Rare Defects: Looking at the Dark Face of the Thrombosis.International journal of environmental research and public health · 2021Review
- Model-dependent contributions of FXII and FXI to venous thrombosis in mice.Journal of thrombosis and haemostasis : JTH · 2020Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe intrinsic pathway factors (F) XII and FXI have been shown to contribute to thrombosis in animal models. We assessed the role of FXII and FXI in venous thrombosis in three distinct mouse models.
methodsVenous thrombosis was assessed in mice genetically deficient for either FXII or FXI. Three models were used: the inferior vena cava (IVC) stasis, IVC stenosis, and femoral vein electrolytic injury models.
resultsIn the IVC stasis model, FXII and FXI deficiency did not affect the size of thrombi but their absence was associated with decreased levels of fibrin(ogen) and an increased level of the neutrophil extracellular trap marker citrullinated histone H3. In contrast, a deficiency of either FXII or FXI resulted in a significant and equivalent reduction in thrombus weight and incidence of thrombus formation in the IVC stenosis model. Thrombi formed in the IVC stenosis model contained significantly higher levels of citrullinated histone H3 compared with the thrombi formed in the IVC stasis model. Deletion of either FXII or FXI also resulted in a significant and equivalent reduction in both fibrin and platelet accumulation in the femoral vein electrolytic injury model.
conclusionsCollectively, these data indicate that FXII and FXI contribute to the size of venous thrombosis in models with blood flow and thrombus composition in a stasis model. This study also demonstrates the importance of using multiple mouse models to assess the role of a given protein in venous thrombosis.
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