ArticleNeural regeneration research2026
Spinal cord injury-derived exosomes exacerbate damage: miR-155-5p mediates inflammatory responses.
Article in Neural regeneration research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Emerging regenerative strategies for spinal cord injury: exosome-derived mechanisms and therapeutic insights.Frontiers in neuroscience · 2025Pooled it
- Extracellular vesicle-based therapeutic strategies for spinal cord injury.Extracellular vesicles and circulating nucleic acids · 2026Review
- Exosome-derived ncRNAs and proteins: inflammation regulatory mechanisms and biomarker potential in spinal cord injury.Frontiers in molecular biosciences · 2026Review
- Exosomes as regenerative therapeutics for spinal cord injury: mechanisms and clinical prospects.Frontiers in medicine · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
JOURNAL/nrgr/04.03/01300535-202606000-00066/figure1/v/2026-02-11T151048Z/r/image-tiff Spinal cord injury is a critical event characterized by intricate pathogenic mechanisms. Although recent studies have highlighted tissue exosomes as key mediators of inflammatory responses in diverse organs and tissues, their role in spinal cord injury has yet to be determined. In this study, we investigated the role and mechanisms of spinal cord tissue exosomes in the inflammatory response following spinal cord injury. We found morphological, concentration, and functional differences between exosomes extracted from injured and normal spinal cord tissues, and identified proinflammatory effects associated with spinal cord injury-generated tissue exosomes but not with exosomes derived from normal spinal cord tissue. Our in vivo and in vitro analyses showed that spinal cord injury-generated tissue exosomes promoted microglial M1 polarization and inflammatory cytokine expression, thereby exacerbating tissue and neuronal injury in the spinal cord. In addition, the combination of exosomal miRNA sequencing and experimental verification showed that the miR-155-5p level was higher in spinal cord injury-generated tissue exosomes than in spinal cord tissue. We further found that spinal cord injury-generated tissue exosomes-derived miR-155-5p induced a significant inhibition of forkhead box O3a phosphorylation and activated the nuclear factor-kappa B pathway, thereby promoting microglial M1 polarization and inflammatory cytokine expression. These findings suggest that injury-induced miR-155-5p-containing exosomes exacerbate spinal cord injury via the promotion of microglial M1 polarization and inflammatory responses. Thus, targeting miR-155-5p expression or exosome secretion could be a novel strategy for attenuating inflammation and reducing secondary injury post-spinal cord injury.
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Registered trials
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