ArticleBlood2015
Endogenous plasminogen activators mediate progressive intracerebral hemorrhage after traumatic brain injury in mice.
Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 126 citations in OpenAlex.
- Therapeutic efficacy of tranexamic acid on traumatic brain injury: a systematic review and meta-analysis.Scandinavian journal of trauma, resuscitation and emergency medicine · 2024Pooled it
- Alpha-defensins: risk factor for thrombosis in COVID-19 infection.British journal of haematology · 2021Trial
- Tranexamic acid to reduce head injury death in people with traumatic brain injury: the CRASH-3 international RCT.Health technology assessment (Winchester, England) · 2021Trial
- Tranexamic acid administration in the field does not affect admission thromboelastography after traumatic brain injury.The journal of trauma and acute care surgery · 2020Trial
- Effects of tranexamic acid on death, disability, vascular occlusive events and other morbidities in patients with acute traumatic brain injury (CRASH-3): a randomised, placebo-controlled trial.Lancet (London, England) · 2019Trial
- Trial
- Longitudinal changes in coagulation-fibrinolysis in patients with traumatic brain injury within seven days after injury.iScience · 2026Article
- Functional Aspects of Fibrin Structure Alterations by Tranexamic Acid in the Inhibition of Fibrinolysis.Biomolecules · 2026Article
- Characterizing the impact of traumatic brain injury phenotype on coagulation dynamics in severely injured patients.Thrombosis research · 2026Article
- Review
- 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
- Tranexamic Acid and Systemic Complement Activation in Traumatic Brain Injury Patients.Journal of the American College of Surgeons · 2025Article
- Disseminated intravascular coagulation.Journal of intensive care · 2025Review
- Hemostatic disturbances in traumatic brain injury: from mechanism to management.Acta neurochirurgica · 2025Review
- Management Challenges in Trauma-Induced Coagulopathy: A Case Report of Hemothorax Requiring Reoperation.The American journal of case reports · 2024Article
- Association of single bolus versus bolus followed by infusion of tranexamic acid with blood loss in adolescent idiopathic scoliosis surgery.Perioperative medicine (London, England) · 2024Article
- Phenotypes of Disseminated Intravascular Coagulation.Thrombosis and haemostasis · 2024Article
- The role of fibrinogen in traumatic brain injury: from molecular pathological mechanisms to clinical management.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2023Review
- Early Posttraumatic Antifibrinolysis Reduces Perioperative Hidden Blood Loss in Elderly Patients with an Intertrochanteric Fracture: A Randomized Controlled Trial.Journal of clinical medicine · 2023Article
- Acute Haemostatic Depletion and Failure in Patients with Traumatic Brain Injury (TBI): Pathophysiological and Clinical Considerations.Journal of clinical medicine · 2023Review
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Persistent intracerebral hemorrhage (ICH) is a major cause of death and disability after traumatic brain injury (TBI) for which no medical treatment is available. Delayed bleeding is often ascribed to consumptive coagulopathy initiated by exposed brain tissue factor. We examined an alternative hypothesis, namely, that marked release of tissue-type plasminogen activator (tPA) followed by delayed synthesis and release of urokinase plasminogen activator (uPA) from injured brain leads to posttraumatic bleeding by causing premature clot lysis. Using a murine model of severe TBI, we found that ICH is reduced in tPA(-/-) and uPA(-/-) mice but increased in PAI-1(-/-) mice compared with wild-type (WT) mice. tPA(-/-), but not uPA(-/-), mice developed a systemic coagulopathy post-TBI. Tranexamic acid inhibited ICH expansion in uPA(-/-)mice but not in tPA(-/-) mice. Catalytically inactive tPA-S(481)A inhibited plasminogen activation by tPA and uPA, attenuated ICH, lowered plasma d-dimers, lessened thrombocytopenia, and improved neurologic outcome in WT, tPA(-/-), and uPA(-/-) mice. ICH expansion was also inhibited by tPA-S(481)A in WT mice anticoagulated with warfarin. These data demonstrate that protracted endogenous fibrinolysis induced by TBI is primarily responsible for persistent ICH and post-TBI coagulopathy in this model and offer a novel approach to interrupt bleeding.
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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.