ArticleHaematologica2020
Extracellular mitochondria released from traumatized brains induced platelet procoagulant activity.
Article in Haematologica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.
What it found
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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.
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Who cites it
31 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Mitochondrial Transfer in the Neurovascular Unit, Not Only for Energy Rescue: A Systematic Review.Aging and disease · 2024Pooled it
- Stress and circulating cell-free mitochondrial DNA: A systematic review of human studies, physiological considerations, and technical recommendations.Mitochondrion · 2021Pooled it
- 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
- Rethinking Mitochondria: The Extracellular Dimension.Circulation research · 2026Review
- Brain-derived microvesicles induce activation of aspirin-treated platelets via the PLC/PKC pathway.Scientific reports · 2026Article
- Unique Pattern of Coagulopathy Among Patients With Severe Traumatic Brain Injury: A Principal Component Analysis of Hemorrhagic Shock Trials.Critical care medicine · 2026Article
- Mitochondria beyond boundaries: from cellular powerhouses to intercellular messengers in health and disease.Science China. Life sciences · 2026Review
- The hidden battlefield: platelet function in the wake of severe trauma.Frontiers in immunology · 2026Review
- Brain rewired: Redox control of brain cell crosstalk via nanotubes and vesicles.Free radical biology & medicine · 2025Review
- Metabolically aberrant extracellular mitochondria induce oxidative endotheliopathy in traumatic brain injury.Blood advances · 2025Article
- Extracellular mitochondria contribute to acute lung injury via disrupting macrophages after traumatic brain injury.Journal of neuroinflammation · 2025Article
- Mitochondrial-Mediated Platelet Activation in Polymyalgia Rheumatica.ACR open rheumatology · 2025Article
- Extracellular vesicles in disorders of hemostasis following traumatic brain injury.Frontiers in neurology · 2024Review
- Article
- Mitochondrial-mediated inflammation and platelet activation in giant cell arteritis.Clinical immunology (Orlando, Fla.) · 2023Article
- Roles and therapeutic potential of different extracellular vesicle subtypes on traumatic brain injury.Cell communication and signaling : CCS · 2023Review
- Role of circulating mitochondria in venous thrombosis in glioblastoma.Journal of thrombosis and haemostasis : JTH · 2023Article
- Platelet-Derived Extracellular Vesicles in Arterial Thrombosis.Advances in experimental medicine and biology · 2023Article
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Coagulopathy often develops soon after acute traumatic brain injury and its cause remains poorly understood. We have shown that injured brains release cellular microvesicles that disrupt the endothelial barrier and induce consumptive coagulopathy. Morphologically intact extracellular mitochondria accounted for 55.2% of these microvesicles, leading to the hypothesis that these extracellular mitochondria are metabolically active and serve as a source of oxidative stress that activates platelets and renders them procoagulant. In testing this hypothesis experimentally, we found that the extracellular mitochondria purified from brain trauma mice and those released from brains subjected to freeze-thaw injury remained metabolically active and produced reactive oxygen species. These extracellular mitochondria bound platelets through the phospholipid-CD36 interaction and induced α-granule secretion, microvesiculation, and procoagulant activity in an oxidant-dependent manner, but failed to induce aggregation. These results define an extracellular mitochondria-induced and redox-dependent intermediate phenotype of platelets that contribute to the pathogenesis of traumatic brain injury-induced coagulopathy and inflammation.
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Registered trials
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