{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T00:47:34Z","timestamp":1787878054648,"version":"build-2784847793"},"reference-count":48,"publisher":"American Society for Clinical Investigation","issue":"21","license":[{"start":{"date-parts":[[2025,11,10]],"date-time":"2025-11-10T00:00:00Z","timestamp":1762732800000},"content-version":"vor","delay-in-days":55,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"crossref","award":["18TPA34230077"],"award-info":[{"award-number":["18TPA34230077"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["R01 DK123694"],"award-info":[{"award-number":["R01 DK123694"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2025,11,10]]},"abstract":"<jats:p>\n                    Fibroblast growth factor receptors (FGFRs) are tyrosine kinase receptors critical for organogenesis and tissue maintenance, including in the adrenal gland. Here we delineate the role of FGFR2 in the morphogenesis, maintenance, and function of the adrenal cortex with a focus on the zona glomerulosa (zG). zG-specific\n                    <jats:italic>Fgfr2<\/jats:italic>\n                    deletion (Fgfr2-cKO) resulted in impaired zG cell identity, proliferation, and transdifferentiation into zona fasciculata (zF) cells during postnatal development. In adult mice, induced deletion of\n                    <jats:italic>Fgfr2<\/jats:italic>\n                    led to loss of mature zG cell identity, highlighting the importance of FGFR2 for the maintenance of a differentiated zG state. Strikingly, Fgfr2-cKO was sufficient to fully abrogate \u03b2-catenin\u2013induced zG hyperplasia and to reduce aldosterone levels. Finally, short-term treatment with pan-FGFR small molecule inhibitors suppressed aldosterone production in both WT and \u03b2-catenin gain-of-function mice. These results demonstrate a critical role for FGFR signaling in adrenal morphogenesis, maintenance, and function and suggest that targeting FGFR signaling may benefit patients with aldosterone excess and\/or adrenal hyperplasia.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.184863","type":"journal-article","created":{"date-parts":[[2025,9,16]],"date-time":"2025-09-16T16:01:01Z","timestamp":1758038461000},"source":"Crossref","is-referenced-by-count":4,"title":["Abrogation of FGFR signaling blocks \u03b2-catenin\u2013induced adrenocortical hyperplasia and aldosterone production"],"prefix":"10.1172","volume":"10","author":[{"given":"Vasileios","family":"Chortis","sequence":"first","affiliation":[{"name":"Division of Endocrinology, Boston Children\u2019s Hospital, Boston, Massachusetts, USA."},{"name":"Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, 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