ArticleJournal of cellular physiology2019
Tranexamic acid suppresses the release of mitochondrial DNA, protects the endothelial monolayer and enhances oxidative phosphorylation.
Article in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- Tranexamic acid administration in the field does not affect admission thromboelastography after traumatic brain injury.The journal of trauma and acute care surgery · 2020Trial
- Tranexamic acid inhibits mitochondrial DNA release and reduces inflammatory response in an in vitro model of OGD/R-induced Caco-2 cell injury.BMC pharmacology & toxicology · 2026Article
- Mitochondria as a Therapeutic Target for Burn Injury.Biomolecules · 2026Review
- Tranexamic Acid-Associated Hyaluronic Acid Exhibits Enhanced Oxidative Stability: A Comparative Rheological Study.Biomolecules · 2026Article
- Establishment and Validation of a C57BL/6J Mouse Model for Melasma.Cell proliferation · 2026Article
- Tranexamic acid and erythropoietin inhibited inflammatory response and endoplasmic reticulum stress and protected rats against acute lung injury caused by osteoporotic hip fracture.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2025Article
- Mitochondrial dysfunction is a major cause of thromboinflammation and inflammatory cell death in critical illnesses.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Tranexamic acid reduces inflammation, edema and burn wound conversion in a rodent model.Burns : journal of the International Society for Burn Injuries · 2024Article
- Fibrinogen Fragment X Mediates Endothelial Barrier Disruption via Suppression of VE-Cadherin.The Journal of surgical research · 2024Article
- Tranexamic acid for haemostasis and beyond: does dose matter?Thrombosis journal · 2023Review
- Comment on "mt-Keima detects PINK1-PRKN mitophagy in vivo with greater sensitivity thanAutophagy · 2021Article
- Trauma-induced coagulopathy.Nature reviews. Disease primers · 2021Review
- Prolonged Cardiopulmonary Bypass is Associated With Endothelial Glycocalyx Degradation.The Journal of surgical research · 2020Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Damage-associated molecular patterns, including mitochondrial DNA (mtDNA) are released during hemorrhage resulting in the development of endotheliopathy. Tranexamic acid (TXA), an antifibrinolytic drug used in hemorrhaging patients, enhances their survival despite the lack of a comprehensive understanding of its cellular mechanisms of action. The present study is aimed to elucidate these mechanisms, with a focus on mitochondria. We found that TXA inhibits the release of endogenous mtDNA from granulocytes and endothelial cells. Furthermore, TXA attenuates the loss of the endothelial monolayer integrity induced by exogenous mtDNA. Using the Seahorse XF technology, it was demonstrated that TXA strongly stimulates mitochondrial respiration. Studies using Mitotracker dye, cells derived from mito-QC mice, and the ActivSignal IPAD assay, indicate that TXA stimulates biogenesis of mitochondria and inhibits mitophagy. These findings open the potential for improvement of the strategies of TXA applications in trauma patients and the development of more efficient TXA derivatives.
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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.