ArticleMolecular neurobiology2024
Edaravone Alleviates Traumatic Brain Injury by Inhibition of Ferroptosis via FSP1 Pathway.
Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Sal-hDPSCs Transplantation Alleviates Hypoxic-Ischaemic Ferroptosis in Neonatal Rats Via the FSP1-CoQInternational dental journal · 2026Article
- Photoacoustic imaging-guided, synchronously targeted thrombolysis and neuroprotection of acute ischemic stroke.iScience · 2026Article
- Edaravone: Advances on cytoprotective effects, pharmacological properties, and mechanisms of action.Pharmacological reviews · 2026Review
- Mechanistic Approach to Ferroptosis in Cancer and Neurological Diseases.Current drug targets · 2026Review
- NLRP3 Inflammasome Activation in Oxidative Stress: A Key Mechanism Driving Neuroinflammation.Neuroimmunomodulation · 2026Review
- Traumatic brain injury-related ferroptosis: current perspectives.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Neutrophil extracellular traps aggravate blood-brain barrier disruption via ZBP1/FSP1-mediated ferroptosis after traumatic brain injury.Fluids and barriers of the CNS · 2025Article
- Ferroptosis in cancer: metabolism, mechanisms and therapeutic prospects.Molecular cancer · 2025Review
- Iron homeostasis and ferroptosis in human diseases: mechanisms and therapeutic prospects.Signal transduction and targeted therapy · 2024Review
- The role of ferroptosis in neurodegenerative diseases.Frontiers in cellular neuroscience · 2024Review
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8 authors.
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Abstract
Traumatic brain injury (TBI) is a highly severe form of trauma with complex series of reactions in brain tissue which ultimately results in neuronal damage. Previous studies proved that neuronal ferroptosis, which was induced by intracranial haemorrhage and other reasons, was one of the most primary causes of neuronal damage following TBI. However, the association between neuronal mechanical injury and ferroptosis in TBI and relevant treatments remain unclear. In the present study, we first demonstrated the occurrence of neuronal ferroptosis in the early stage of TBI and preliminarily elucidated that edaravone (EDA), a cerebroprotective agent that eliminates oxygen radicals, was able to inhibit ferroptosis induced by TBI. A cell scratching model was established in PC12 cells, and it was confirmed that mechanical injury induced ferroptosis in neurons at the early stage of TBI. Ferroptosis suppressor protein 1 (FSP1) plays a significant role in inhibiting ferroptosis, and we found that iFSP, a ferroptosis agonist which is capable to inhibit FSP1 pathway, attenuated the anti-ferroptosis effect of EDA. In conclusion, our results suggested that EDA inhibited neuronal ferroptosis induced by mechanical injury in the early phase of TBI by activating FSP1 pathway, which could provide evidence for future research on prevention and treatment of TBI.
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