ArticleFrontiers in immunology2025
FOXA2/miR-148a-3p/SMURF2 signaling feed-forward loop alleviates spinal cord ischemia-reperfusion injury-induced neuropathic pain by modulating microglia polarization in rats.
Article in Frontiers in immunology, 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.
- Microbiota-derived 4-HPAA alleviates Crohn's disease by stabilizing SIRT1 and reprogramming macrophage immunometabolism.Apoptosis : an international journal on programmed cell death · 2026Article
- Neuropathic Pain: Mapping the miRNA Landscape.Non-coding RNA · 2026Review
- The mechanism of dynamic switching between M1/M2 phenotypes of microglia in neuropathic pain: a narrative review.Frontiers in molecular neuroscience · 2026Review
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9 authors.
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Abstract
Background: Microglia polarization is crucial in mediating neuropathic pain. However, the role of microglia polarization in regulating spinal cord ischemia-reperfusion injury (SCIRI)-induced neuropathic pain is largely unknown. This study aimed to elucidate the relationship between SCIRI-induced neuropathic pain and microglia polarization, as well as the underlying mechanisms, with the objective of identifying potential therapeutic targets. Methods: A rat model of SCIRI was established by aortic arch clamping, then pain thresholds were measured. Results: SCIRI significantly reduced mechanical and thermal pain thresholds in rats and promoted microglial polarization, with a concomitant decrease in SIRT1 expression and an increase in SMURF2 expression in microglial cells. Further analysis revealed that upregulation of miR-148a-3p promoted microglia polarization toward M2 by targeting SMURF2, which in turn inhibited ubiquitination of SIRT1. FOXA2 was an upstream transcription factor of miR-148a-3p and SMURF2 bound to FOXA2, resulting in its ubiquitination. Finally, Conclusions: The FOXA2/miR-148a-3p/SMURF2 signaling feed-forward loop regulates SIRT1 levels and thereby exerts control over microglia polarization and the regulation of SCIRI-induced neuropathic pain.
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