ArticleJournal of translational medicine2025
Stage-specific transcriptomic alterations in the spinal cord reveal key regulatory genes and potential therapeutic targets in a rat model of neuropathic pain.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Activating Transcription Factor 3 in Pain: A Molecular Regulator and Emerging Biomarker.Genes · 2026Review
- Effects of FGF4/HIF-1α axis-mediated neuronal glycolysis on neuropathic pain.The journal of headache and pain · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeuropathic pain is a prevalent chronic pain condition with complex pathogenesis, posing significant challenges due to its diverse etiologies and limited treatment options. We aim to analyze different stage transcriptomic changes to identify potential molecular targets for guiding future research and treatment of neuropathic pain.
methodsSpinal cords were collected from rats subjected to chronic constriction injury surgery (CCI) at 0.5, 1, 3, 7, and 14 days post-injury. RNA sequencing was performed (n = 3 per group), followed by differential gene expression analysis, pathway enrichment analysis, and protein-protein interaction analysis. The differentially expressed genes identified were validated using quantitative real-time PCR. TAK-242 were intrathecally administered to pharmacological inhibit Ly86, mechanical allodynia and thermal hyperalgesia were evaluated in chronic constriction injury rats.
resultsSignificant changes in differentially expressed genes enriched in immune, metabolic, and inflammatory pathways were observed at various time points, particularly during the stabilization phase (7 and 14 days post-chronic constriction injury), with 529 and 352 differentially expressed genes identified at these respective time points. Notably, genes related to the complement pathway, neurotrophic factors, and lysosomal functions were consistently upregulated, suggesting their potential roles in neuropathic pain pathogenesis. Protein-protein interaction network analysis identified key regulatory genes, including Clec12a, Ly86, Ctsz, and Fcgr3a, which could be potential therapeutic targets for neuropathic pain. Inhibition of Ly86 alleviated pain in CCI mice, confirming its role as a critical modulator of neuropathic pain. These findings may contribute to the development of targeted therapies for human neuropathic pain.
conclusionsOur findings provide valuable insights into the molecular mechanisms underlying neuropathic pain and may contribute to the development of more effective treatment strategies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.