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Increasing evidence indicates that mitochondrial dysfunction and metabolic stress critically influence inflammatory responses. However, the mechanistic link between mitochondrial impairment and persistent neuroinflammation in NP remains incompletely understood.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A peripheral nerve injury model was used to induce NP in mice. Mitochondrial integrity, mitochondrial DNA (mtDNA) release, and activation of the cGAS-STING-IRF3 pathway were examined in the spinal cord using immunofluorescence, molecular analyses, and single-cell RNA sequencing. Genetic silencing of CMPK2 was achieved by adeno-associated virus delivery, and pharmacological inhibition was performed using nordihydroguaiaretic acid (NDGA). Pain-related behaviors were assessed in vivo. Complementary in vitro experiments were conducted in BV2 cells and primary microglia to evaluate mitochondrial function and mtDNA-driven innate immune activation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Peripheral nerve injury induced mitochondrial damage in the spinal cord, accompanied by cytosolic mtDNA release and activation of cGAS-STING-IRF3 signaling. IRF3 was observed to associate with the CMPK2 promoter and regulate CMPK2 transcription, consistent with a potential feedback mechanism that may exacerbate mitochondrial stress, enhance mtDNA release, and sustain innate immune activation. Single-cell RNA sequencing and immunofluorescence analyses revealed that CMPK2 was expressed in multiple spinal cord cell types, with microglia representing a major population contributing to CMPK2 upregulation in the spinal dorsal horn after nerve injury. Genetic silencing or pharmacological inhibition of CMPK2 was associated with reduced cGAS-STING signaling, improved mitochondrial homeostasis, decreased microglial activation, and attenuation of NP-like behaviors in vivo. Consistently, CMPK2 knockdown in microglia attenuated mtDNA-induced innate immune activation and improved mitochondrial function in vitro.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>These findings support a model in which an mtDNA-cGAS-STING-IRF3-CMPK2-associated immunometabolic feedback mechanism operates within the spinal cord microenvironment, with notable microglial involvement, linking mitochondrial dysfunction to sustained neuroinflammation and NP. Targeting mitochondrial immunometabolism may represent a potential therapeutic strategy for chronic inflammatory conditions characterized by persistent innate immune activation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12967-026-08314-8","type":"journal-article","created":{"date-parts":[[2026,5,22]],"date-time":"2026-05-22T06:28:34Z","timestamp":1779431314000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Mitochondrial DNA release contributes to neuropathic pain via a cGAS-STING-IRF3-CMPK2-associated immunometabolic feedback mechanism"],"prefix":"10.1186","volume":"24","author":[{"given":"Bo","family":"Wang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hui","family":"Zeng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongrui","family":"Zhan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yin","family":"Xu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ziwei","family":"Hu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiahui","family":"Pang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhichao","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yan","family":"Ma","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5576-2999","authenticated-orcid":false,"given":"Wen","family":"Wu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,5,22]]},"reference":[{"key":"8314_CR1","doi-asserted-by":"publisher","first-page":"2204","DOI":"10.1016\/j.pain.2011.06.017","volume":"152","author":"TS Jensen","year":"2011","unstructured":"Jensen TS, Baron R, Haanp\u00e4\u00e4 M, Kalso E, Loeser JD, Rice ASC, Treede RD. 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