{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,28]],"date-time":"2026-07-28T22:45:25Z","timestamp":1785278725693,"version":"3.55.0"},"reference-count":73,"publisher":"American Society for Clinical Investigation","issue":"6","license":[{"start":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T00:00:00Z","timestamp":1773619200000},"content-version":"vor","delay-in-days":48,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"NIH","award":["2R01DK123694"],"award-info":[{"award-number":["2R01DK123694"]}]},{"DOI":"10.13039\/501100001711","name":"Swiss National Science Foundation","doi-asserted-by":"crossref","award":["310030L_182700\/1"],"award-info":[{"award-number":["310030L_182700\/1"]}],"id":[{"id":"10.13039\/501100001711","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"crossref","award":["26POST1569366"],"award-info":[{"award-number":["26POST1569366"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,3,16]]},"abstract":"<jats:p>\n                    How \u03b2-catenin (\u03b2Cat) mediates tissue hyperplasia is poorly understood. To explore this, we employed the adrenal cortex as a model system given its stereotypical spatial organization and the important role \u03b2Cat plays in homeostasis and disease. For example, excessive production of aldosterone by the adrenal cortex (primary aldosteronism [PA]) is a major cause of cardiovascular morbidity and is associated with \u03b2Cat gain of function (\u03b2Cat-GOF). Adherens junctions (AJs) connect the actin cytoskeletons of adjacent zona glomerulosa (zG) cells via a cadherin\u2013\u03b2Cat\u2013\u03b1-catenin complex and mediate aldosterone production. Whether \u03b2Cat-GOF drives zG hyperplasia, a key feature of PA, via AJs is unknown. Here, we showed that aldosterone secretagogues (K\n                    <jats:sup>+<\/jats:sup>\n                    and AngII) and \u03b2Cat-GOF mediated AJ formation via Rho\/ROCK\/actomyosin signaling. In addition, Rho\/ROCK inhibition led to altered zG rosette morphology and decreased aldosterone production. Mice with zG-specific \u03b2Cat-GOF demonstrated increased AJ formation and zG hyperplasia, which was blunted by Rho\/ROCK inhibition and deletion of \u03b1-catenin (\u03b1Cat). \u03b2Cat also impacted AJ formation independently of its role as a transcription factor. Furthermore, analysis of human aldosterone-producing adenomas revealed high levels of \u03b2Cat expression were associated with increased membranous expression of K-cadherin. Together, our findings identified Rho\/ROCK signaling and \u03b1Cat as key mediators of AJ formation and \u03b2Cat-driven hyperplasia.\n                  <\/jats:p>","DOI":"10.1172\/jci196271","type":"journal-article","created":{"date-parts":[[2026,1,27]],"date-time":"2026-01-27T17:00:53Z","timestamp":1769533253000},"source":"Crossref","is-referenced-by-count":2,"title":["Rho\/ROCK signaling and \u03b1-catenin mediate \u03b2-catenin\u2013driven hyperplasia in the adrenal cortex via adherens junctions"],"prefix":"10.1172","volume":"136","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2157-2158","authenticated-orcid":true,"given":"Mesut","family":"Berber","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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Switzerland."},{"name":"Medizinische Klinik und Poliklinik IV, Klinikum der Universit\u00e4t, Ludwig-Maximilians-Universit\u00e4t, Munich, Germany."},{"name":"The LOOP Zurich Medical Research Center, Zurich, Switzerland."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Diana L.","family":"Carlone","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Boston Children\u2019s Hospital, Boston, Massachusetts, USA."},{"name":"Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA."},{"name":"Harvard Stem Cell Institute, Cambridge, Massachusetts, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David T.","family":"Breault","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Boston Children\u2019s Hospital, Boston, Massachusetts, USA."},{"name":"Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA."},{"name":"Harvard Stem Cell Institute, Cambridge, Massachusetts, 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