ArticleResearch and practice in thrombosis and haemostasis2022
Tissue factor release following traumatic brain injury drives thrombin generation.
Article in Research and practice in thrombosis and haemostasis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Pathway-level proteomics identifies subcellular trafficking dysregulation as a molecular signature in severe traumatic brain injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Primary Blast-Induced Traumatic Brain Injury as a Risk Factor for (Cerebro)vascular Disorder: Clinical Manifestations, Blast Physics, Biomechanics, Pathobiology, and Critical Gaps.International journal of molecular sciences · 2026Review
- The Association of the Neutrophil-to-Lymphocyte Ratio and the D-dimer-to-Albumin Ratio with Deep Vein Thrombosis in Patients with Spontaneous Intracerebral Hemorrhage.International journal of general medicine · 2026Article
- Risk warning of systemic immune-inflammation index and coagulation parameters for hospital-acquired pneumonia in patients with traumatic brain injury.American journal of translational research · 2026Article
- The hidden battlefield: platelet function in the wake of severe trauma.Frontiers in immunology · 2026Review
- Protease-activated receptor 4 deficiency increases mortality, intracranial bleeding, and blood-brain barrier impairment following traumatic brain injury in mice.Research and practice in thrombosis and haemostasis · 2025Article
- Hemostatic disturbances in traumatic brain injury: from mechanism to management.Acta neurochirurgica · 2025Review
- Hemogram-Based Phenotypes of the Immune Response and Coagulopathy in Blunt Thoracic Trauma.Journal of personalized medicine · 2024Article
- Risk factors for thromboembolic complications in isolated severe head injury.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2024Article
- A Machine Learning Model Based on CT Imaging Metrics and Clinical Features to Predict the Risk of Hospital-Acquired Pneumonia After Traumatic Brain Injury.Infection and drug resistance · 2024Article
- Extracellular vesicles in disorders of hemostasis following traumatic brain injury.Frontiers in neurology · 2024Review
- Detection of tissue factor-positive extracellular vesicles using the ExoView R100 system.Research and practice in thrombosis and haemostasis · 2023Article
- Tissue factor release following traumatic brain injury drives thrombin generation.Research and practice in thrombosis and haemostasis · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Background: Traumatic brain injury (TBI) results in neurovascular damage that initiates intrinsic mechanisms of hypercoagulation, which can contribute to the development of life-threatening complications, such as coagulopathy and delayed thrombosis. Clinical studies have hypothesized that tissue factor (TF) induces hypercoagulability after TBI; however, none have directly shown this relationship. Objectives: In the current study, we took a stepwise approach to understand what factors are driving thrombin generation following experimental TBI. Methods: We employed the contusion-producing controlled cortical impact (CCI) model and the diffuse closed head injury (CHI) model to investigate these mechanisms as a function of injury severity and modality. Whole blood was collected at 6 hours and 24 hours after injury, and platelet-poor plasma was used to measure thrombin generation and extracellular vesicle (EV) TF. Results: We found that plasma thrombin generation, dependent on TF present in the plasma, was greater in CCI-injured animals compared to sham at both 6 hours (120.4 ± 36.9 vs 0.0 ± 0.0 nM*min endogenous thrombin potential) and 24 hours (131.0 ± 34.0 vs 32.1 ± 20.6 nM*min) after injury. This was accompanied by a significant increase in EV TF at 24 hours (328.6 ± 62.1 vs 167.7 ± 20.8 fM) after CCI. Further, EV TF is also increased at 6 hours (126.6 ± 17.1 vs 63.3 ± 14.4 fM) but not 24 hours following CHI. Conclusion: TF-mediated thrombin generation is time-dependent after injury and TF increases resolve earlier following CHI as compared to CCI. Taken together, these data support a TF-mediated pathway of thrombin generation after TBI and pinpoint TF as a major player in TBI-induced coagulopathy.
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Registered trials
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