ArticleScience advances2025
Athlete-derived extracellular vesicles protect against spinal cord injury via inhibition of neuronal ferroptosis.
Article in Science advances, 2025. 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.
- "Membrane-Guided" Repair Strategy: Precision Delivery of GGT1 Degrader for Targeted Repair and Regeneration of Spinal Cord Neurons.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The role of OTUD1-mediated deubiquitination in disease pathogenesis: from molecular mechanisms to clinical translation.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
- 3D bioprinted multifunctional GelMA/TMP scaffold integrated with neural stem cell-derived extracellular vesicles and neural progenitor cells for spinal cord injury repair.Journal of tissue engineeringArticle
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cord injury (SCI) causes high morbidity, disability, and mortality, while current surgical and pharmacological treatments provide limited benefit. Ferroptosis, a newly recognized form of regulated cell death, contributes critically to SCI pathology, and targeting this process may enhance neuronal survival. Extracellular vesicles, key mediators of intercellular communication, are emerging as promising therapeutic agents for central nervous system injury. Here, we examined the role of athlete-derived plasma extracellular vesicles (AEVs) in neuronal ferroptosis and motor function recovery after SCI. In a murine model, AEVs markedly inhibited ferroptosis and improved motor outcomes. Mechanistically, AEVs delivered RNF216, which promoted ubiquitination and degradation of NOX1, thereby reducing ferroptotic damage and facilitating recovery. Moreover, RNF216-enriched vesicles enhanced synaptic plasticity, supporting neuronal regeneration and network reestablishment. These findings reveal a previously unrecognized RNF216-NOX1 axis in SCI and highlight AEVs as a previously unidentified therapeutic strategy.
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Registered trials
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