Wei, Yu-SyuanYu-SyuanWeiCheng, Hui-PingHui-PingChengCHING-HO WUYEN-CHEN CHANGLin, Ruo-WeiRuo-WeiLinYU-TING HSUYI-TING CHENSHUEI-LIONG LINSU-YI TSAISHINN-CHIH WUPEI-SHIUE TSAI2022-06-202022-06-202022-03-302227-9059https://scholars.lib.ntu.edu.tw/handle/123456789/613123https://www.scopus.com/inward/record.uri?eid=2-s2.0-85128293596&doi=10.3390%2fbiomedicines10040810&partnerID=40&md5=9b38a2b83065a8a6a3d75d8ccd4622a6Being one of the renal replacement therapies, peritoneal dialysis (PD) maintains around 15% of end-stage kidney disease patients' lives; however, complications such as peritoneal fibrosis and ultrafiltration failure during long-term PD compromise its application. Previously, we established a sodium hypochlorite (NaClO)-induced peritoneal fibrosis porcine model, which helped to bridge the rodent model toward pre-clinical human peritoneal fibrosis research. In this study, the peritoneal equilibration test (PET) was established to evaluate instant functional changes in the peritoneum in the pig model. Similar to observations from long-term PD patients, increasing small solutes transport and loss of sodium sieving were observed. Mechanistic investigation from both in vivo and in vitro data suggested that disruption of cytoskeleton induced by excessive reactive oxygen species defected intracellular transport of aquaporin 1, this likely resulted in the disappearance of sodium sieving upon PET. Functional interference of aquaporin 1 on free water transport would result in PD failure in patients.enaquaporin; cytoskeleton; oxidative stress; peritoneal dialysis; porcine[SDGs]SDG3Oxidative Stress-Induced Alterations of Cellular Localization and Expression of Aquaporin 1 Lead to Defected Water Transport upon Peritoneal Fibrosisjournal article10.3390/biomedicines10040810354535602-s2.0-85128293596WOS:000786250300001https://scholars.lib.ntu.edu.tw/handle/123456789/609467