ArticleBMC medicine2026
Unraveling the neurotoxic mechanisms of tranexamic acid in epilepsy induction: a network toxicology and molecular docking approach.
Article in BMC medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Potential Mechanisms Linking Excessive Testosterone to PMOS: Insights from Network Toxicology and Machine Learning.Metabolites · 2026Article
- Network toxicology and bioinformatics reveal potential molecular links between cadmium exposure and pancreatic cancer.BMC pharmacology & toxicology · 2026Article
- Computational pharmacovigilance of tranexamic acid: implications for intracerebral hemorrhage based on FAERS database and network toxicology.Frontiers in pharmacology · 2026Article
- From empirical hemostasis to precision reversal: clinical challenges, technological innovations, and individualized strategies in anticoagulant-associated bleeding.Frontiers in cardiovascular medicine · 2026Review
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Authors and funding
6 authors.
Funding
Abstract
backgroundTranexamic acid, an antifibrinolytic drug, is effective for surgical hemostasis and bleeding-related disorders but may induce neurotoxicity, such as epilepsy. The mechanisms driving TXA-induced epilepsy remain poorly understood, as traditional toxicology approaches fall short in capturing its complex toxicity profile. This study employs network toxicology and molecular docking to elucidate the multi-target molecular mechanisms of TXA-induced epilepsy, aiming to enhance its safe clinical application.
methodsTXA toxicity was predicted using ADMETlab2.0, PROTOX3.0, toxCSM, and ADMET-AI, with SMILES sequences obtained from PubChem, and a TXA target library was constructed using databases such as ChEMBL. EP-related targets were screened from databases such as GeneCards, and target intersections were analyzed using R software. Networks were constructed using Cytoscape and STRING, with GO and KEGG analyses performed to investigate molecular pathways. Molecular docking was conducted using the CB-Dock2 platform to analyze TXA binding to core targets.
resultsTXA poses a neurotoxicity risk, with 51 intersecting targets identified between TXA and EP, among which GABRA1, GABBR2, GABRA5, GABRA2, and GAD1 exhibited the greatest relevance. Analysis revealed that TXA induces EP by disrupting GABA signaling and synaptic function. The PPI network confirmed five core targets, and GO and KEGG analyses elucidated their roles in neural suppression. Molecular docking demonstrated stable binding of TXA to these targets, with Vina scores ranging from - 5.2 to - 6.9.
conclusionThis study elucidates the mechanisms of TXA-induced EP through network toxicology and molecular docking, confirming its interference with GABA-related targets and neural suppression functions. The study overcomes the limitations of traditional toxicology, providing a scientific basis for the safe use of TXA and prevention of neurotoxicity.
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