Research Advances on M2 Microglia in Neuropathic Pain

Corresponding author: huangchangshun, fyyhuangchangshun@nbu.edu.cn

DOI: 10.12201/bmr.202603.00106

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  Abstract: Neuropathic pain (NP) is a chronic pain condition caused by damage to central or peripheral nerves, characterized by complex mechanisms and limited treatment efficacy. Microglia, as specialized immune cells of the central nervous system, play a crucial role in the development and progression of NP. M1 (pro-inflammatory) microglia recruit immune cells by releasing pro-inflammatory factors such as TNF-α, IL-1β, and IL-6, thereby exacerbating neuroinflammation and promoting pain progression. In contrast, M2 (anti-inflammatory) microglia promote nerve repair by secreting anti-inflammatory factors like IL-4 and IL-10, as well as neurotrophic factors such as IGF-1 and BDNF, exerting crucial neuroprotective effects. Therefore, regulating microglial polarization toward the M2 phenotype represents a therapeutic strategy for NP. Based on this, this review summarizes the neuroprotective mechanisms of M2 microglia in NP and reviews research progress on related signaling pathways, providing new insights and potential directions for clinical intervention in NP.

  Key words: Neuropathic pain; M2 Microglia; Neuroprotection; signal pathways

  Submit time: 24 March 2026

  Copyright: The copyright holder for this preprint is the author/funder, who has granted biomedRxiv a license to display the preprint in perpetuity.
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