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Here, we found that in the corneas of\n                    <jats:italic>Aqp5<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    mice at older than 6 months, loss of AQP5 significantly increased corneal neovascularization, inflammatory cell infiltration, and corneal haze. The results of immunofluorescence staining showed that upregulation of K1, K10, and K14, and downregulation of K12 and Pax6 were detected in\n                    <jats:italic>Aqp5<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    cornea and primary corneal epithelial cells. Loss of AQP5 aggravated wound\u2010induced corneal neovascularization, inflammation, and haze. mRNA sequencing, western blotting, and qRT\u2010PCR showed that Wnt2 and Wnt6 were significantly decreased in\n                    <jats:italic>Aqp5<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    corneas and primary corneal epithelial cells, accompanied by decreased aggregation in the cytoplasm and nucleus of \u03b2\u2010catenin. IIIC3 significantly suppressed corneal neovascularization, inflammation, haze, and maintained corneal transparent epithelial in\n                    <jats:italic>Aqp5<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    corneas. We also found that pre\u2010stimulated\n                    <jats:italic>Aqp5<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    primary corneal epithelial cells with IIIC3 caused the decreased expression of K1, K10, and K14, the increased expression of K12, Pax6, and increased aggregation in the cytoplasm and nucleus of \u03b2\u2010catenin. These findings revealed that AQP5 may regulate corneal epithelial homeostasis and function through the Wnt\/\u03b2\u2010catenin signaling pathway. Together, we uncovered a possible role of AQP5 in determining corneal epithelial cell fate and providing a potential therapeutic target for corneal epithelial dysfunction.\n                  <\/jats:p>","DOI":"10.1096\/fj.202201503r","type":"journal-article","created":{"date-parts":[[2023,1,23]],"date-time":"2023-01-23T09:45:13Z","timestamp":1674467113000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Loss of aquaporin 5 contributes to the corneal epithelial pathogenesis via Wnt\/\u03b2\u2010catenin pathway"],"prefix":"10.1096","volume":"37","author":[{"given":"Yihui","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Human Anatomy, Histology and Embryology School of Basic Medicine, Qingdao University  Qingdao 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