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Beyond inflammation: a comprehensive microglial regulation model in chronic pain
Yu Lei1, Qian Wang1, Feixiang Wang2
1Department of Anesthesiology, Guangyuan Central Hospital, Guangyuan, 628000, Sichuan, China.
Molecular Biology Reports
|September 15, 2025
Summary
Microglia, immune cells in the brain, drive chronic pain through neuroinflammation and maladaptive plasticity. Targeting specific microglial states offers new therapeutic avenues for pain chronification.
Area of Science:
- Neuroscience
- Immunology
- Pain Research
Background:
- Chronic pain involves persistent neuroimmune dysregulation, with microglia central to maladaptive plasticity.
- Microglial activation sustains central sensitization, even without peripheral injury, via epigenetic, metabolic, and synaptic mechanisms.
Purpose of the Study:
- To present a comprehensive framework for microglial regulation in chronic pain.
- To explore the failure of immune tolerance and aberrant neuron-glia signaling in pain chronification.
- To discuss targeted therapeutic strategies for microglial phenotypes.
Main Methods:
- Review of current literature on microglial function in chronic pain.
- Analysis of epigenetic, metabolic, and synaptic modulation by microglia.
- Examination of therapeutic interventions targeting microglial pathways.
Main Results:
- Microglia contribute to chronic pain through complex, multidimensional processes beyond classical inflammation.
- Dysregulated neuron-glia signaling and failed immune tolerance perpetuate microglial activation.
- Specific microglial states are identified as key drivers of pain chronification.
Conclusions:
- Microglia are dynamic regulators, not just inflammatory mediators, in chronic pain.
- Targeting microglial epigenetic, metabolic, or signaling pathways shows therapeutic potential.
- Understanding microglial dysregulation is crucial for developing effective chronic pain treatments.
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