ArticleBlood2021
Conformation-dependent blockage of activated VWF improves outcomes of traumatic brain injury in mice.
Article in Blood, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
What it found
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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
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Prognostic value of von Willebrand factor and ADAMTS13 in patients with COVID-19: A systematic review and meta-analysis.Thrombosis research · 2022Pooled it
- Von Willebrand factor A2 domain inhibits A1-DNA binding while preserving A1-platelet interaction under flow: evidence from recombinant domain constructs.Research and practice in thrombosis and haemostasis · 2026Article
- Hyperadhesive von Willebrand Factor Contributes to Pathogenesis of Preeclampsia.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Longitudinal changes in coagulation-fibrinolysis in patients with traumatic brain injury within seven days after injury.iScience · 2026Article
- A commentary on "The role of coagulopathy and subdural hematoma thickness at admission in predicting the prognoses of patients with severe traumatic brain injury: a multicenter retrospective cohort study from China".International journal of surgery (London, England) · 2026Article
- Vicinal disulfide bond modulates A1-GPIbα interaction by altering the force-induced conformational changes of A2 domain.Communications biology · 2025Article
- Key residues regulating von Willebrand factor A1/A2 interactions: insights from molecular dynamics simulations and experimental validation.Research and practice in thrombosis and haemostasis · 2025Article
- Sexually Dimorphic Responses Reveal Multifaceted Benefits of Glibenclamide in Traumatic Brain Injury.Journal of neurotrauma · 2025Article
- Metabolically aberrant extracellular mitochondria induce oxidative endotheliopathy in traumatic brain injury.Blood advances · 2025Article
- β2 integrin regulates neutrophil trans endothelial migration following traumatic brain injury.Cell communication and signaling : CCS · 2025Article
- Single-nucleus RNA sequencing-based construction of a hippocampal neuron atlas in mice with epileptic cognitive impairment.iScience · 2024Article
- The effect of ADAMTS13 on graft-versus-host disease.Journal of cellular and molecular medicine · 2024Article
- Roles and therapeutic potential of different extracellular vesicle subtypes on traumatic brain injury.Cell communication and signaling : CCS · 2023Review
- Extracellular vesicles, hyperadhesive von willebrand factor, and outcomes of gastric cancer: a clinical observational study.Medical oncology (Northwood, London, England) · 2023Observational
- Removal of the vicinal disulfide enhances the platelet-capturing function of von Willebrand factor.Blood · 2023Article
- Article
- Selective sphingosine-1-phosphate receptor 1 modulator attenuates blood-brain barrier disruption following traumatic brain injury by inhibiting vesicular transcytosis.Fluids and barriers of the CNS · 2022Article
- Brain-Derived Extracellular Vesicles Induce Vasoconstriction and Reduce Cerebral Blood Flow in Mice.Journal of neurotrauma · 2022Article
- Hyperadhesive von Willebrand Factor Promotes Extracellular Vesicle-Induced Angiogenesis: Implication for LVAD-Induced Bleeding.JACC. Basic to translational science · 2022Article
- Article
Corrections and comments
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Authors and funding
16 authors at 7 institutions in 2 countries.
Funding
Abstract
Traumatic brain injury-induced coagulopathy (TBI-IC) causes life-threatening secondary intracranial bleeding. Its pathogenesis differs mechanistically from that of coagulopathy arising from extracranial injuries and hemorrhagic shock, but it remains poorly understood. We report results of a study designed to test the hypothesis that von Willebrand factor (VWF) released during acute TBI is intrinsically hyperadhesive because its platelet-binding A1-domain is exposed and contributes to TBI-induced vascular leakage and consumptive coagulopathy. This hyperadhesive VWF can be selectively blocked by a VWF A2-domain protein to prevent TBI-IC and to improve neurological function with a minimal risk of bleeding. We demonstrated that A2 given through intraperitoneal injection or IV infusion reduced TBI-induced death by >50% and significantly improved the neurological function of C57BL/6J male mice subjected to severe lateral fluid percussion injury. A2 protected the endothelium from extracellular vesicle-induced injury, reducing TBI-induced platelet activation and microvesiculation, and preventing a TBI-induced hypercoagulable state. A2 achieved this therapeutic efficacy by specifically blocking the A1 domain exposed on the hyperadhesive VWF released during acute TBI. These results suggest that VWF plays a causal role in the development of TBI-IC and is a therapeutic target for this life-threatening complication of TBI.
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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.