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However, the transcriptional networks that orchestrate this maladaptive plasticity remain largely undefined. Here, we identify the transcriptional repressor ZBTB18 as a critical regulator of this pathogenic process. Peripheral nerve injury markedly downregulated the level of ZBTB18 in the injured trigeminal ganglion (TG) of rats.\u00a0Restoring ZBTB18 expression reverses injury\u2010induced mechanical allodynia, while its knockdown in naive TG neurons is sufficient to recapitulate neuropathic pain symptoms. Mechanistically, ZBTB18 directly represses\u00a0\n                    <jats:italic>Clic1<\/jats:italic>\n                    \u00a0transcription by engaging a specific silencer element within its promoter. This repression is achieved through the recruitment of the nucleosome remodeling and deacetylase (NuRD) complex, an interaction mediated by the ZBTB18 BTB domain and the chromodomain helicase DNA\u2010binding protein 4 (CHD4). Disruption of this recruitment abrogates histone H3K27ac deacetylation at the\u00a0\n                    <jats:italic>Clic1<\/jats:italic>\n                    \u00a0promoter, enhancing RNA polymerase II occupancy and driving\n                    <jats:italic>Clic1<\/jats:italic>\n                    expression. Consequently, nerve injury\u2010induced loss of ZBTB18 relieves this epigenetic brake, leading to CLIC1 upregulation, increased chloride channel activity, and hyperexcitability of TG neurons that underlies mechanical hypersensitivity. In summary, these findings reveal a novel ZBTB18\/NuRD\/CLIC1 epigenetic axis in neuropathic pain and highlight this transcriptional pathway as a potential target for therapeutic intervention.\n                  <\/jats:p>","DOI":"10.1002\/advs.77364","type":"journal-article","created":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T15:16:06Z","timestamp":1787843766000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["ZBTB18 Dysfunction Promotes Neuropathic Pain via CHD4\u2010based Epigenetic Disinhibition of CLIC1 Channels in Sensory Neurons"],"prefix":"10.1002","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8578-2133","authenticated-orcid":false,"given":"Shoupeng","family":"Wang","sequence":"first","affiliation":[{"name":"The First Affiliated Hospital of Soochow University School of Basic Medical Sciences Suzhou Medical College of Soochow University  Suzhou People's Republic of 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