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Nevertheless, long\u2010term exposure to PD fluid can damage the peritoneal membrane, leading to ultrafiltration failure and, ultimately, discontinuation of PD. Investigation of the molecular mechanisms underlying this damage is essential for identifying new therapeutic targets to mitigate peritoneal deterioration in PD patients. To this end, we employed RNA sequencing in a preclinical model of peritoneal injury, induced by prolonged chlorhexidine (CHX) exposure, which revealed cytosolic DNA\u2010sensing signaling as a novel pathway. Next, we demonstrated that key players in this pathway, such as the stimulator of interferon genes (STING) and its downstream signaling effectors (interferon regulatory factor 3, interferon\u2010stimulated genes, and nuclear factor\u2010\u03baB signaling), were upregulated in experimental peritoneal damage. Moreover, increased STING expression was observed in human peritoneal biopsies from patients with PD. Subsequent studies in STING\u2010deficient mice showed reduced proinflammatory gene expression and immune cell infiltration, together with inhibited nuclear factor\u2010\u03baB pathway activation at both early (10\u2009days) and late (30\u2009days) stages of CHX\u2010induced peritoneal injury. STING deficiency also reduced peritoneal membrane thickening, fibrosis, and mesothelial\u2010to\u2010mesenchymal transition (MMT)\u2010related changes in advanced CHX\u2010induced damage. Furthermore, pharmacological inhibition of STING with C\u2010176 attenuated CHX\u2010induced peritoneal inflammation. Macrophages were identified as one of the STING\u2010expressing cell types in the injured peritoneum. Hence,\n                    <jats:italic>in vitro<\/jats:italic>\n                    STING blockade in activated macrophages inhibited MMT in cultured mesothelial cells, suggesting that STING activation in this population may drive peritoneal fibrosis. Additionally, STING deficiency reduced peritoneal inflammation in\n                    <jats:italic>S. epidermidis<\/jats:italic>\n                    \u2010induced peritonitis and decreased adhesion scores in a postsurgical intra\u2010abdominal adhesion model. These findings identify STING as a pivotal mediator of peritoneal injury and support its potential as a novel therapeutic target to prevent PD\u2010associated ultrafiltration failure. \u00a9 2025 The Author(s).\n                    <jats:italic>The Journal of Pathology<\/jats:italic>\n                    published by John Wiley &amp; Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.\n                  <\/jats:p>","DOI":"10.1002\/path.6462","type":"journal-article","created":{"date-parts":[[2025,8,14]],"date-time":"2025-08-14T11:32:37Z","timestamp":1755171157000},"page":"196-212","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["<scp>STING<\/scp>\n                    inhibition alleviates experimental peritoneal damage: potential therapeutic relevance for peritoneal dialysis"],"prefix":"10.1002","volume":"267","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2767-0229","authenticated-orcid":false,"given":"Vanessa","family":"Marchant","sequence":"first","affiliation":[{"name":"Cellular and Molecular Biology in Renal and Vascular Pathology Laboratory Health Research Institute\u2010Fundaci\u00f3n Jim\u00e9nez D\u00edaz University Hospital, Universidad Aut\u00f3noma de Madrid (IIS\u2010FJD, UAM)  Madrid Spain"},{"name":"RICORS2040  Madrid Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jorge","family":"Garc\u00eda\u2010Gim\u00e9nez","sequence":"additional","affiliation":[{"name":"RICORS2040  Madrid Spain"},{"name":"Laboratory of Nephrology and Hypertension Health Research Institute\u2010Fundaci\u00f3n Jim\u00e9nez D\u00edaz University Hospital, Universidad Aut\u00f3noma de Madrid (IIS\u2010FJD, UAM)  Madrid Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guadalupe T","family":"Gonz\u00e1lez\u2010Mateo","sequence":"additional","affiliation":[{"name":"Tissue and Organ Homeostasis Program, Centro de Biolog\u00eda Molecular Severo Ochoa (CBM), CSIC \u2010 Universidad Aut\u00f3noma de Madrid  Madrid Spain"},{"name":"Premium Research, S.L.  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