ArticleBlood2016
A novel role for von Willebrand factor in the pathogenesis of experimental cerebral malaria.
Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Contribution of a European-Prevalent Variant near CD83 and an East Asian-Prevalent Variant near IL17RB to Herpes Zoster Risk in Tofacitinib Treatment: Results of Genome-Wide Association Study Meta-Analyses.Arthritis & rheumatology (Hoboken, N.J.) · 2021Pooled it
- CCL5 and CD11b-fibrin interactions regulate microglia migration and morphology in hyperinflammatory experimental cerebral malaria.Journal of neuroinflammation · 2026Article
- Mouse models to study von Willebrand factor in inflammation: a scoping review.Intensive care medicine experimental · 2026Review
- LL-37 selectively targets Plasmodium-infected erythrocytes and exhibits antimalarial activity.PLoS pathogens · 2026Article
- Structure and multiple functions of von Willebrand factor.Haematologica · 2026Review
- Severe Plasmodium Falciparum Malaria Mimicking Thrombotic Thrombocytopenic Purpura (TTP): A Case Report From China.International medical case reports journal · 2025Article
- Novel functions for von Willebrand factor.Blood · 2024Review
- Deciphering the triad of endothelial glycocalyx, von Willebrand Factor, and P-selectin in inflammation-induced coagulation.Frontiers in cell and developmental biology · 2024Review
- Article
- von Willebrand factor links primary hemostasis to innate immunity.Nature communications · 2022Article
- Hemostatic and protein C pathway dysfunction in the pathogenesis of experimental cerebral malaria.Haematologica · 2022Article
- Antithrombin protects against Plasmodium falciparum histidine-rich protein II-mediated inflammation and coagulation.Blood advances · 2022Article
- Functional changes in hemostasis during asexual and sexual parasitemia in a controlled human malaria infection.PloS one · 2022Article
- The von Willebrand factor - ADAMTS-13 axis in malaria.Research and practice in thrombosis and haemostasis · 2022Article
- Age-Associated Increase in Thrombogenicity and Its Correlation with von Willebrand Factor.Journal of clinical medicine · 2021Review
- ADAMTS13 regulation of VWF multimer distribution in severe COVID-19.Journal of thrombosis and haemostasis : JTH · 2021Article
- Illustrated State-of-the-Art Capsules of the ISTH 2020 Congress.Research and practice in thrombosis and haemostasis · 2021Review
- The relationship between ABO blood group, von Willebrand factor, and primary hemostasis.Blood · 2020Review
- Low VWF: insights into pathogenesis, diagnosis, and clinical management.Blood advances · 2020Review
- More on 'Association between ABO blood groups and risk of SARS-CoV-2 pneumonia'.British journal of haematology · 2020Article
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Authors and funding
14 authors at 7 institutions in 4 countries.
Funding
Abstract
Plasmodium falciparum malaria infection is associated with an early marked increase in plasma von Willebrand factor (VWF) levels, together with a pathological accumulation of hyperreactive ultra-large VWF (UL-VWF) multimers. Given the established critical role of platelets in malaria pathogenesis, these increases in plasma VWF raise the intriguing possibility that VWF may play a direct role in modulating malaria pathogenesis. To address this hypothesis, we used an established murine model of experimental cerebral malaria (ECM), in which wild-type (WT) C57BL/6J mice were infected with Plasmodium berghei ANKA. In keeping with findings in children with P falciparum malaria, acute endothelial cell activation was an early and consistent feature in the murine model of cerebral malaria (CM), resulting in significantly increased plasma VWF levels. Despite the fact that murine plasma ADAMTS13 levels were not significantly reduced, pathological UL-VWF multimers were also observed in murine plasma following P berghei infection. To determine whether VWF plays a role in modulating the pathogenesis of CM in vivo, we further investigated P berghei infection in VWF(-/-) C57BL/6J mice. Clinical ECM progression was delayed, and overall survival was significantly prolonged in VWF(-/-) mice compared with WT controls. Despite this protection against ECM, no significant differences in platelet counts or blood parasitemia levels were observed between VWF(-/-) and WT mice. Interestingly, however, the degree of ECM-associated enhanced blood-brain barrier permeability was significantly attenuated in VWF(-/-) mice compared with WT controls. Given the significant morbidity and mortality associated with CM, these novel data may have direct translational significance.
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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.