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This study aimed to investigate the roles of peroxisome proliferator-activated receptor gamma (PPAR\u03b3) in PF pathogenesis.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>Rat and cellular PF models were established by high glucose dialysate and lipopolysaccharide treatments. Serum creatinine, urea nitrogen, and glucose contents were detected by ELISA. Histological evaluation was done through H&amp;E and Masson staining. GLUT1, PPAR\u03b3, and other protein expression were measured by qRT-PCR, western blotting, and IHC. PPAR\u03b3 and GLUT1 subcellular distribution were detected using confocal microscopy. Cell proliferation was assessed by MTT and Edu staining.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>Serum creatinine, urea nitrogen and glucose, and PPAR\u03b3 and GLUT1 expression in rat PF model were reduced by PPAR\u03b3 agonists Rosiglitazone or 15d-PGJ2 and elevated by antagonist GW9662. Rosiglitazone or 15d-PGJ2 repressed and GW9662 aggravated peritoneal fibrosis in rat PF model. PPAR\u03b3 and GLUT1 were mainly localized in nucleus and cytosols of peritoneal mesothelial cells, respectively, which were reduced in cellular PF model, enhanced by Rosiglitazone or 15d-PGJ2, and repressed by GW9662. TGF-\u03b2 and a-SMA expression was elevated in cellular PF model, which was inhibited by Rosiglitazone or 15d-PGJ2 and promoted by GW9662. PPAR\u03b3 silencing reduced GLUT1, elevated a-SMA and TGF-b expression, and promoted peritoneal mesothelial cell proliferation, which were oppositely changed by PPAR\u03b3 overexpression.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusion<\/jats:title>\n                <jats:p>PPAR\u03b3 inhibited high glucose-induced peritoneal fibrosis progression through elevating GLUT1 expression and repressing peritoneal mesothelial cell proliferation.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1007\/s11010-022-04419-y","type":"journal-article","created":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T04:09:28Z","timestamp":1649131768000},"page":"1959-1971","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["PPAR\u03b3 alleviates peritoneal fibrosis progression along with promoting GLUT1 expression and suppressing peritoneal mesothelial cell proliferation"],"prefix":"10.1007","volume":"477","author":[{"given":"Junxia","family":"Feng","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Meizhi","family":"Lu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wenhao","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jingchun","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ping","family":"Meng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zukai","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuejuan","family":"Gao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9966-5023","authenticated-orcid":false,"given":"Yunfang","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2022,4,5]]},"reference":[{"key":"4419_CR1","doi-asserted-by":"publisher","first-page":"1692","DOI":"10.3389\/fphys.2018.01692","volume":"9","author":"AC Raby","year":"2018","unstructured":"Raby AC, Labeta MO (2018) Preventing peritoneal dialysis-associated fibrosis by therapeutic blunting of peritoneal toll-like receptor activity. 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