{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T10:15:33Z","timestamp":1783505733383,"version":"3.55.0"},"reference-count":79,"publisher":"BMJ","funder":[{"DOI":"10.13039\/100000065","name":"NINDS","doi-asserted-by":"crossref","award":["R01NS121144"],"award-info":[{"award-number":["R01NS121144"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Foundation for Anesthesia Education and Research Mentored Research"}],"content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["Reg Anesth Pain Med"],"accepted":{"date-parts":[[2026,6,22]]},"abstract":"<jats:sec>\n                    <jats:title>Background\/importance<\/jats:title>\n                    <jats:p>Neuropathic pain affects up to 10% of the population and is often refractory to current treatments. Growing evidence implicates neuroimmune interactions, particularly microglia, in the pathophysiology, but their role is underappreciated in clinical practice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To summarize current evidence for microglial contributions to neuropathic pain, emphasizing microglia\u2013neuron interactions and translational implications for clinicians.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Evidence review<\/jats:title>\n                    <jats:p>This narrative review synthesizes preclinical and emerging human data (postmortem histopathology, glial-signal positron emission tomography (PET) imaging, dorsal root ganglion transcriptomics) to examine microglial contributions to pain initiation, maintenance and resolution, sex differences and therapeutic implications.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Findings<\/jats:title>\n                    <jats:p>Preclinical evidence demonstrates that microglia are necessary and sufficient for pain initiation. Nerve injury engages central sensitization through colony-stimulating factor 1 (CSF1)\u2013CSF1 receptor (CSF1R), purinergic receptors, damage-associated molecular pattern\/Toll-like receptor signaling, cytokine cascades (TNF\u03b1, IL-1\u03b2, IL-6), prostaglandin E\u2082, extracellular matrix and synaptic remodeling and brain-derived neurotrophic factor\u2013tropomyosin receptor kinase B-mediated disinhibition. Microglia also contribute to pain resolution via pro-resolving mediators and stimulator of interferon genes (STING)\/interferon signaling. Sex differences are prominent: microglial mechanisms predominate in males, whereas T-cell-mediated pathways prevail in females. Human postmortem and glial-signal imaging studies support glial involvement in chronic pain but lack direct validation of specific microglial targets.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Microglia coordinate pain initiation and resolution via conserved, drug-addressable pathways. Three translational implications emerge: (1) neuroimmune interventions are most effective early, given that microglia drive initiation more than maintenance; (2) sex-stratified trial designs are warranted given divergent microglial versus T-cell mechanisms by sex and (3) CSF1R-PET imaging may enable mechanism-based patient selection. These implications require prospective clinical validation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/rapm-2026-107844","type":"journal-article","created":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T09:30:11Z","timestamp":1783503011000},"page":"rapm-2026-107844","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["Neuropathic pain through the perspective of microglia\u2013neuron interactions: a translational review for clinicians"],"prefix":"10.1136","author":[{"given":"Lingyi","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Anesthesiology, Sun Yan-sen University of Medical Sciences, Guangzhou, Guangdong, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jessica","family":"Yu","sequence":"additional","affiliation":[{"name":"Department of Anesthesia and Perioperative Care, University of California San Francisco, San Francisco, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaobing","family":"Yu","sequence":"additional","affiliation":[{"name":"Department of Anesthesia and Perioperative Care, University of California San Francisco, San Francisco, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5992-8370","authenticated-orcid":false,"given":"Zhonghui","family":"Guan","sequence":"additional","affiliation":[{"name":"Department of Anesthesia and Perioperative Care, University of California San Francisco, San Francisco, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0003-8696","authenticated-orcid":false,"given":"Po-Yi Paul","family":"Su","sequence":"additional","affiliation":[{"name":"Department of Anesthesia and Perioperative Care, University of California San Francisco, San Francisco, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"239","published-online":{"date-parts":[[2026,7,8]]},"reference":[{"key":"2026070802300790000_rapm-2026-107844v1.1","unstructured":"Institute of Medicine (US) Committee on Advancing Pain Research, Care, and Education . 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