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We investigated whether persistent YAP\/TAZ alveolar epithelial cell signaling contributes to failed epithelial repair and persistent fibrotic remodeling. In IPF lungs, we identified increased YAP\n                    <jats:sup>+<\/jats:sup>\n                    TAZ\n                    <jats:sup>+<\/jats:sup>\n                    alveolar epithelial cells and increased transcriptional target expression. Pharmacological YAP\/TAZ activation in human alveolar epithelial cell organoids and in murine AT2 cell organoids generated with genetic YAP\/TAZ activation (YT\n                    <jats:sup>active<\/jats:sup>\n                    ) (via deletion of Hippo kinases\n                    <jats:italic>Stk3<\/jats:italic>\n                    and\n                    <jats:italic>Stk4<\/jats:italic>\n                    ) resulted in phenotype shifts into aberrant transitional and airway-like states. Bleomycin injury of YT\n                    <jats:sup>active<\/jats:sup>\n                    mice resulted in persistent fibrotic remodeling at 28 and 56 days after bleomycin injury. Gene promoter activity associated with transitional cell markers (\n                    <jats:italic>Krt19<\/jats:italic>\n                    ,\n                    <jats:italic>Hopx<\/jats:italic>\n                    , and\n                    <jats:italic>Runx2<\/jats:italic>\n                    ) was increased in YT\n                    <jats:sup>active<\/jats:sup>\n                    AT2 cells. Immunofluorescent staining showed a loss of AT2-associated Cebpa and increased\n                    <jats:italic>Krt19<\/jats:italic>\n                    in YT\n                    <jats:sup>active<\/jats:sup>\n                    lineage-traced AT2 cells 28 days after injury. Inhibition of YAP\/TAZ using verteporfin resulted in improved lung repair in YT\n                    <jats:sup>active<\/jats:sup>\n                    mouse lungs, including restored Cebpa and decreased\n                    <jats:italic>\n                      Krt19\n                      <jats:sup>+<\/jats:sup>\n                    <\/jats:italic>\n                    transitional cells. These findings demonstrate that sustained YAP\/TAZ activation drives abnormal alveolar repair and persistent fibrotic remodeling. Blocking aberrant persistent YAP\/TAZ activity promotes adaptive repair and has potential as a therapeutic strategy for pulmonary fibrosis.\n                  <\/jats:p>\n                  <jats:p>Persistent alveolar epithelial YAP\/TAZ activity leads to abnormal transitional cell differentiation and failed alveolar repair that promotes development and progression of pulmonary fibrosis.<\/jats:p>","DOI":"10.1172\/jci.insight.198113","type":"journal-article","created":{"date-parts":[[2026,6,9]],"date-time":"2026-06-09T16:01:05Z","timestamp":1781020865000},"source":"Crossref","is-referenced-by-count":4,"title":["Sustained YAP\/TAZ activation promotes aberrant alveolar epithelial cell differentiation and drives persistent fibrotic remodeling"],"prefix":"10.1172","volume":"11","author":[{"given":"Isabella P.","family":"Gaona","sequence":"first","affiliation":[{"name":"Division of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1944-220X","authenticated-orcid":true,"given":"A. 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