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Microglial metabolic reprogramming and neuroinflammation drive NP progression. Although ChREBP (key metabolic regulator) protects against NP, its specific mechanisms remain unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>NP rat model was established via spared nerve injury (SNI) surgery, and mechanical allodynia was evaluated using Von Frey tests. ChREBP expression in microglia was detected through immunofluorescence, RT\u2010qPCR, and western blot. Functional studies involved ChREBP knockdown\/overexpression to assess effects on microglial polarization, neuroinflammation, neuronal excitability, pain behaviors, and fatty acid metabolism. Mechanisms were explored via dual\u2010luciferase reporter and chromatin immunoprecipitation assays.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Mechanical pain thresholds were significantly decreased on the ipsilateral side after SNI. ChREBP was upregulated in SDH microglia after SNI and in LPS\u2010stimulated microglia in\u00a0vitro. ChREBP knockdown inhibited anti\u2010inflammatory microglial polarization, exacerbated neuroinflammation, and aggravated pain. Conversely, ChREBP overexpression promoted the anti\u2010inflammatory phenotype, suppressed neuroinflammation, and alleviated pain. ChREBP enhanced microglial fatty acid oxidation and energy metabolism. Mechanistically, ChREBP bound to the TFBS1 site on the PGC\u20101\u03b1 promoter to activate its transcription. PGC\u20101\u03b1 overexpression rescued the impairments caused by ChREBP knockdown, including reduced fatty acid oxidation, suppressed anti\u2010inflammatory polarization, elevated inflammatory factors, and increased neuronal excitability. The protective effects of ChREBP were attenuated by the fatty acid oxidation inhibitor Etomoxir.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>ChREBP alleviates NP by enhancing microglial fatty acid oxidation and anti\u2010inflammatory phenotype via PGC\u20101\u03b1 transcriptional activation, revealing a novel metabolic\u2010immune axis for potential NP therapy.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/cns.70744","type":"journal-article","created":{"date-parts":[[2026,1,10]],"date-time":"2026-01-10T08:36:27Z","timestamp":1768034187000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["<scp>PGC<\/scp>\n                    \u20101\u03b1 Transcriptionally Regulated by\n                    <scp>ChREBP<\/scp>\n                    Mitigates Neuropathic Pain Through Promoting Microglial Fatty Acid Oxidation and Anti\u2010Inflammatory Response"],"prefix":"10.1002","volume":"32","author":[{"given":"Ziwei","family":"Hu","sequence":"first","affiliation":[{"name":"Center of Rehabilitation Medicine, Zhujiang Hospital Southern Medical University  Guangzhou China"},{"name":"School of Rehabilitation Sciences Southern Medical University  Guangzhou China"},{"name":"Guang Dong Engineering Technology Research Center of Brain Function Assessment and Neuroregulation Rehabilitation  Guangzhou China"},{"name":"Institute of Exercise and Rehabilitation Science, Zhujiang Hospital Southern Medical University  Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiahui","family":"Pang","sequence":"additional","affiliation":[{"name":"Center of Rehabilitation Medicine, Zhujiang Hospital Southern Medical University  Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xinli","family":"Liu","sequence":"additional","affiliation":[{"name":"Center 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