ArticleJCI insight2023
Neutrophil extracellular traps contribute to coagulopathy after traumatic brain injury.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.
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Who cites it
38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 39 citations in OpenAlex.
- Investigating the Role of Neutrophil Extracellular Traps as a Therapeutic Target in Traumatic Brain Injury: a Systematic Review and Meta-analysis.Molecular neurobiology · 2025Pooled it
- The Diagnostic, Therapeutic and Prognostic Relevance of Neutrophil Extracellular Traps in Polytrauma.Biomolecules · 2023Pooled it
- Association Between Platelet Transfusion and ICU Mortality Within 28 Days Among Patients With Intracranial Hemorrhage Complicated by Thrombocytopenia: A Propensity Score-Matched Cohort Study.Medical science monitor : international medical journal of experimental and clinical research · 2026Article
- Analysis of the Relationship between Early Clinical Factors and Glasgow Outcome Scale in Patients With Traumatic Brain Injury.Brain and behavior · 2026Article
- Hallmarks of the multidimensional immune response to trauma in humans.Nature immunology · 2026Review
- Evolution of neutrophil extracellular traps in the pathology of stroke.Neural regeneration research · 2026Article
- A 'Tangled Web' in the CNS: unraveling neutrophil extracellular traps in neurological disorders.Molecular neurodegeneration · 2026Review
- Temporal patterns of neutrophil recruitment and microthrombus formation in fatal traumatic brain injury: a forensic histopathological study.Forensic science, medicine, and pathology · 2026Article
- CD177⁺ neutrophil-platelet aggregates contribute to thromboinflammation via NETs in necrotizing enterocolitis.Nature communications · 2026Article
- Mitochondria beyond boundaries: from cellular powerhouses to intercellular messengers in health and disease.Science China. Life sciences · 2026Review
- Glucocorticoids and Neutrophil Biology: Impact on the Development of Resistance to Glucocorticoid Therapy.Neuroimmunomodulation · 2026Review
- Lipopolysaccharide and HMGB1: key regulatory factors in the pathophysiology of sepsis a mechanistic and therapeutic review.Frontiers in immunology · 2026Review
- 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
- Neutrophil extracellular traps promote neuronal ferroptosis through STING-mediated AMPK dysregulation after traumatic brain injury.International journal of biological sciences · 2026Article
- Advances in cellular and molecular mechanisms of trauma-induced organ inflammation and dysfunction.Burns & trauma · 2026Review
- The mechanism of S100A8/A9 heterodimer promoting atherosclerotic thrombosis.Clinical and experimental medicine · 2025Article
- SOCS2 alleviates traumatic brain injury-induced mitochondrial damage and parthanatos in endothelial cells by inhibiting the JAK2/STAT3 signaling pathway.Metabolic brain disease · 2025Article
- BCL2A1‑ and G0S2‑driven neutrophil extracellular traps: A protective mechanism linking preeclampsia to reduced breast cancer risk.Oncology reports · 2025Article
- Astrocyte-derived CCL5-mediated CCR5Science advances · 2025Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coagulopathy contributes to the majority of deaths and disabilities associated with traumatic brain injury (TBI). Whether neutrophil extracellular traps (NETs) contribute to an abnormal coagulation state in the acute phase of TBI remains unknown. Our objectives were to demonstrate the definitive role of NETs in coagulopathy in TBI. We detected NET markers in 128 TBI patients and 34 healthy individuals. Neutrophil-platelet aggregates were detected in blood samples from TBI patients and healthy individuals using flow cytometry and staining for CD41 and CD66b. Endothelial cells were incubated with isolated NETs and we detected the expression of vascular endothelial cadherin, syndecan-1, thrombomodulin, von Willebrand factor, phosphatidylserine, and tissue factor. In addition, we established a TBI mouse model to determine the potential role of NETs in TBI-associated coagulopathy. NET generation was mediated by high mobility group box 1 (HMGB1) from activated platelets and contributed to procoagulant activity in TBI. Furthermore, coculture experiments indicated that NETs damaged the endothelial barrier and caused these cells to assume a procoagulant phenotype. Moreover, the administration of DNase I before or after brain trauma markedly reduced coagulopathy and improved the survival and clinical outcome of mice with TBI.
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