{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T04:16:14Z","timestamp":1787026574141,"version":"build-2736575974"},"reference-count":146,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,6,17]],"date-time":"2026-06-17T00:00:00Z","timestamp":1781654400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>\n                    Wilson disease (WD) has long been framed as a hepatocentric disorder of copper accumulation. That view is now giving way to a broader model centered on the gut\u2013liver\u2013kidney\u2013brain axis. In WD, copper is not simply stored in tissues as an inert burden. It circulates in dynamic, bioactive pools\u2014particularly relative exchangeable copper (REC)\u2014that disrupt barrier structures, including the intestinal epithelium and blood\u2013brain barrier, and spread toxicity through measurable biochemical mediators. Major pathogenic processes include copper-induced suppression of autophagy, disruption of FXR-regulated bile acid signaling, and direct injury to the intestinal barrier. Gut dysbiosis, supported by fecal microbiota transplantation (FMT) studies in ATP7B-deficient mice, further amplifies hepatic inflammation and favors copper retention. Renal tubular dysfunction and neurotoxicity appear to reflect copper species-dependent passage across biological barriers together with secondary metabolic disturbances, including the recently described pathway of cuproptosis. In the clinic, this shift has been accompanied by greater use of copper-species biomarkers such as ceruloplasmin oxidase activity and REC, along with advanced imaging approaches such as\n                    <jats:sup>64<\/jats:sup>\n                    Cu-PET\/CT. Treatment is also moving beyond conventional chelation alone, with increasing attention to biliary copper excretion, epithelial barrier repair, and microbiome-directed interventions. Viewed in this way, the axis model helps explain the marked phenotypic heterogeneity of WD and offers a mechanistic basis for more precise interventions aimed at breaking pathogenic feedback loops across organs.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2026.1840716","type":"journal-article","created":{"date-parts":[[2026,6,17]],"date-time":"2026-06-17T04:50:40Z","timestamp":1781671840000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["The gut-liver-kidney-brain axis in Wilson disease: copper speciation-flux and barrier-mediated organ crosstalk"],"prefix":"10.3389","volume":"17","author":[{"given":"Nannan","family":"Qian","sequence":"first","affiliation":[{"name":"Department of Neurology, The First Affiliated Hospital of Anhui University of ChineseMedicine","place":["Hefei, Anhui, China"]},{"name":"Graduate School, Anhui University of Chinese Medicine","place":["Hefei, Anhui, 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