ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2025
Pharmacological and Genetic Approaches to Downregulate FIS1 Mitigate Neuropathic Pain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Hierarchical Studies in TRAP2 Mice Demonstrate that Neuronal Activation and Mitochondrial Networks Integration Constitute the Key Mechanism Underlying Painful Syncope.Neuroscience bulletin · 2026Article
- Applications of micro/nano drug delivery systems in cancer pain management.Bioactive materials · 2026Review
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19 authors.
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Abstract
Despite the established link between neuropathic pain and abnormal mitochondrial fission in neurons, the specific role of mitochondrial fission protein 1 (FIS1) in this process remains to be fully elucidated. In this study, the subjects we investigated were 6-8-week-old male mice. Comprehensive behavioral tests and immunostaining, along with Western blot analysis, revealed that neuropathic pain induced by spared nerve injury (SNI) upregulated FIS1 expression in the spinal cord dorsal horn (SC-DH). Furthermore, artificially upregulated FIS1 in SC-DH caused hyperalgesia behaviors in normal mice, while downregulation alleviated neuropathic pain. Using GAD2-MITO and vGluT2-MITO transgenic mice, we found that mitochondria network of both excitatory and inhibitory neurons in the SC-DH were disrupted. Selective downregulation of FIS1 in excitatory neurons via vGluT2-Cre mice reversed mitochondrial impairments and alleviated neuropathic pain. Network pharmacological prediction analysis combined with pharmacological tests indicated that compounds capable of downregulating FIS1 expression, such as epigallocatechin gallate, the primary bioactive component of tea polyphenols, may possess analgesic properties. In contrast, cinnamic acid, an organic acid derived from cinnamon bark, did not exhibit the capability to downregulate FIS1 expression and consequently lacked analgesic efficacy. Our research findings suggest that FIS1 may represent a novel molecular target for the treatment of neuropathic pain.
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