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Transglutaminase 2 (TG2) stabilizes the extracellular matrix against proteases. In an animal model, inhibition of TG2 reduced peritoneal fibrosis, angiogenesis, and inflammation. We investigated the expression of TG2 in 163 human peritoneal membrane tissue samples, including controls, tissues exposed to conventional acidic or low\u2010glucose degradation product (GDP) pH\u2010neutral solutions, and those with peritonitis or encapsulating peritoneal sclerosis (EPS), and explored the role of TG2 in high\u2010glucose\u2013induced pathophysiology in mesothelial cells. TG2 expression was upregulated in association with peritoneal membrane injury and was the highest in peritonitis. TG2 expression was correlated with peritoneal membrane thickness, CD68\u2010positive macrophages, and myofibroblast expression. TG2 was expressed in mesothelial cells, \u03b1\u2010smooth muscle actin\u2010positive myofibroblast expression, macrophages, and endothelial cells in the diseased state. In cultured mesothelial cells, high\u2010glucose\u2013induced upregulation of collagen 1, TGF\u2010\u03b21, and TG2 was suppressed by a TG2 inhibitor or by TGF\u2010\u03b21 small interfering RNA. TG2 is involved in the development of peritoneal injury during PD. High\u2010glucose dialysate is involved in the induction of peritoneal fibrosis through the interactive regulation of TGF\u2010\u03b2 and TG2. Targeting TG2 may offer therapeutic potential for managing PD complications and EPS.<\/jats:p>","DOI":"10.14814\/phy2.70567","type":"journal-article","created":{"date-parts":[[2025,9,22]],"date-time":"2025-09-22T09:48:16Z","timestamp":1758534496000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Transglutaminase 2 in human peritoneal dialysis\u2010related peritoneal injury"],"prefix":"10.14814","volume":"13","author":[{"given":"Shunnosuke","family":"Kunoki","sequence":"first","affiliation":[{"name":"Department of Nephrology and Rheumatology Aichi Medical University  Nagakute Aichi Japan"},{"name":"Department of Endocrinology Metabolism and Nephrology, Nippon Medical School  Tokyo Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masashi","family":"Ikeno","sequence":"additional","affiliation":[{"name":"Department of Medical Cell Biology Aichi Medical University  Nagakute Aichi 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