ArticleBlood2018
Lactadherin promotes microvesicle clearance to prevent coagulopathy and improves survival of severe TBI mice.
Article in Blood, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04274777 (The Relationship Between Lipid Peroxidation Products From Traumatic Brain Injury and Secondary Coagulation Disorders), which is not on this map. Cited by 47 papers.
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.
The Relationship Between Lipid Peroxidation Products From Traumatic Brain Injury and Secondary Coagulation Disorders
Who cites it
47 citing papers in PubMed, 92 citations in OpenAlex.
- Extracellular Mitochondria Mediate Endothelial Injury After Traumatic Brain Injury.Arteriosclerosis, thrombosis, and vascular biology · 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
- The Dual Roles of Extracellular Vesicle Subtypes in Regulating Traumatic Brain Injury.International journal of molecular sciences · 2026Review
- Hematopoietic cell kinase regulates microglial/macrophage activation to drive neuroinflammation after traumatic brain injury.Cell communication and signaling : CCS · 2026Article
- The emerging role of brain-derived microparticles in trauma-induced coagulopathy after traumatic brain injury.Frontiers in neurology · 2026Review
- Targeting hypercoagulability in ischemic stroke modulates fibrin-driven microglial polarization via JAK-STAT pathway.Journal of neuroinflammation · 2025Article
- CD147-high extracellular vesicles promote gastric cancer metastasis via VEGF/AKT/eNOS and AKT/mTOR pathways.Oncogenesis · 2025Article
- Trauma-Induced Coagulopathy: A Review of Specific Molecular Mechanisms.Diagnostics (Basel, Switzerland) · 2025Review
- Injury induced endotheliopathy: overview, diagnosis, and management.Current opinion in critical care · 2025Review
- Hemostatic disturbances in traumatic brain injury: from mechanism to management.Acta neurochirurgica · 2025Review
- Metabolically aberrant extracellular mitochondria induce oxidative endotheliopathy in traumatic brain injury.Blood advances · 2025Article
- Extracellular particles: emerging insights into central nervous system diseases.Journal of nanobiotechnology · 2025Review
- 3,3'-Diindolylmethane improves pathology and neurological outcome following traumatic brain injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Traumatic brain injury: Advances in coagulopathy (Review).Biomedical reports · 2024Review
- Yin-Yang: two sides of extracellular vesicles in inflammatory diseases.Journal of nanobiotechnology · 2024Review
- Extracellular vesicles in disorders of hemostasis following traumatic brain injury.Frontiers in neurology · 2024Review
- Cerebral glucagon-like peptide-1 receptor activation alleviates traumatic brain injury by glymphatic system regulation in mice.CNS neuroscience & therapeutics · 2023Article
- Roles and therapeutic potential of different extracellular vesicle subtypes on traumatic brain injury.Cell communication and signaling : CCS · 2023Review
- Shedding Light on the Cell Biology of Platelet-Derived Extracellular Vesicles and Their Biomedical Applications.Life (Basel, Switzerland) · 2023Review
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Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
Abstract
Coagulopathy is common in patients with traumatic brain injury (TBI) and predicts poor clinical outcomes. We have shown that brain-derived extracellular microvesicles, including extracellular mitochondria, play a key role in the development of TBI-induced coagulopathy. Here, we further show in mouse models that the apoptotic cell-scavenging factor lactadherin, given at a single dose of 400 μg/kg 30 minutes before (preconditioning) or 30 minutes after cerebral fluid percussion injury, prevented coagulopathy as defined by clotting time, fibrinolysis, intravascular fibrin deposition, and microvascular bleeding of the lungs. Lactadherin also reduced cerebral edema, improved neurological function, and increased survival. It achieved these protective effects by enhancing the clearance of circulating microvesicles through phosphatidylserine-mediated phagocytosis. Together, these results identify the scavenging system for apoptotic cells as a potential therapeutic target to prevent TBI-induced coagulopathy and improve the outcome of TBI.
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What OpenQuestion holds
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.