ArticleCNS neuroscience & therapeutics2025
Vimentin Inhibits Neuronal Apoptosis After Spinal Cord Injury by Enhancing Autophagy.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- cGAS-STING pathway modulation: A new hope for neural regeneration.Neural regeneration research · 2026Article
- Anoikis: To Die or Not to Die?International journal of molecular sciences · 2026Review
- Machine Learning Identifies FLNA as a Key Molecular Target Regulating Neuronal Apoptosis after Spinal Cord Injury.Journal of molecular neuroscience : MN · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
aimsNeuron death is caused primarily by apoptosis after spinal cord injury (SCI). Autophagy, as a cellular response, can maintain cellular homeostasis to reduce apoptosis. We aimed to investigate the effect and the mechanism of vimentin knockdown on autophagy and neural recovery after SCI.
methodsThe SD rats with T10 complete transection as SCI model were used. The vimentin RNAi adenovirus was constructed and transplanted into T10 rats with total transection injury of the spinal cord, and the recovery of neurological and motor functions after SCI was evaluated by BBB score, footprint analysis, electrophysiological tests, and immunofluorescence staining. Protein and gene expression were assessed by Western blotting, CO-IP, q-PCR, and immunofluorescence. In addition, neuron-like PC12 cells were infected with adenovirus to further elucidate the effect of vimentin on autophagy and the molecular mechanism of neuronal apoptosis after SCI.
resultsInhibition of SCI induced-vimentin upregulation improved motor function, enhanced the recovery of autophagy flux, and reduced neuronal apoptosis. Notably, this may be related to the formation of vimentin-14-3-3-Beclin1 complex and PI3K class III complex.
conclusionOur results suggest that inhibition of vimentin expression may enhance autophagy and anti-apoptosis in neurons after SCI by affecting the formation of the vimentin-14-3-3-Beclin1 complex, thereby promoting neuronal recovery.
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