{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,25]],"date-time":"2026-08-25T11:21:52Z","timestamp":1787656912079,"version":"build-2736575974"},"reference-count":54,"publisher":"Oxford University Press (OUP)","issue":"18","license":[{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,8,25]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Mutations in CAV3, encoding caveolin-3, cause caveolinopathies, rare genetic disorders affecting both skeletal and cardiac muscle. Caveolin-3 contributes to T-tubule formation and excitation-contraction coupling. To date, there are no therapy for caveolinopathies. BIN1 (amphiphysin 2), a membrane-shaping protein critical for T-tubule integrity, has shown therapeutic promise in congenital myopathies and heart dysfunction. We evaluated the therapeutic impact of BIN1 overexpression in Cav-3 knockout mice, a model recapitulating key features of human caveolinopathy. We assessed skeletal and cardiac function, T-tubule morphology, mitochondria, and gene expression using histological, physiological, and molecular approaches. Results: We found Cav-3\u2212\/\u2212 mice displayed skeletal muscle weakness, T-tubule disorganization, and mitochondrial abnormalities, alongside cardiac diastolic dysfunction and myofibrillar disarray. While BIN1 overexpression failed to improve muscle strength, T-tubule structure, or fiber atrophy, it corrected nuclear positioning and partially restored mitochondrial markers in skeletal muscle. In contrast, BIN1 robustly rescued cardiac performance, restoring end-diastolic volume, cardiac output, and sarcomeric integrity. Expression profiling revealed greater dysregulation of excitation-contraction coupling and atrogene pathways in skeletal than in cardiac muscle in Cav-3\u2212\/\u2212 mice. Cavin-4, a BIN1-interacting protein and caveolar component, was selectively dysregulated in Cav-3\u2212\/\u2212 muscle, suggesting a mechanistic barrier to BIN1-mediated rescue in this tissue. These findings identify tissue-specific differences in the molecular consequences of caveolin-3 loss and demonstrate that BIN1 overexpression effectively rescues cardiac manifestations of caveolinopathy while only partially ameliorating the associated subcellular defects in skeletal muscle. Our results support BIN1 investigation as a potential target for inherited cardiomyopathies, while highlighting the need for alternative strategies in skeletal muscle.<\/jats:p>","DOI":"10.1093\/hmg\/ddag082","type":"journal-article","created":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T11:50:07Z","timestamp":1787313007000},"source":"Crossref","is-referenced-by-count":0,"title":["BIN1 overexpression rescues cardiac but not skeletal muscle defects in a mouse model of caveolinopathy"],"prefix":"10.1093","volume":"35","author":[{"given":"Alice","family":"Moncheaux","sequence":"first","affiliation":[{"name":"Institute of Genetics and Molecular and Cellular Biology (IGBMC), INSERM U1258, CNRS UMR7104, University of Strasbourg , 1 rue Laurent Fries, 67404, 1 rue Laurent Fries, 67404, Illkirch ,","place":["France"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alain","family":"Guimond","sequence":"additional","affiliation":[{"name":"Institut Clinique de la Souris, PHENOMIN-ICS , Phenotyping Department, 1 rue Laurent Fries, 67404, Illkirch ,","place":["France"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Coralie","family":"Spiegelhalter","sequence":"additional","affiliation":[{"name":"Institute of Genetics and Molecular and Cellular Biology (IGBMC), INSERM U1258, CNRS UMR7104, University of Strasbourg , 1 rue Laurent Fries, 67404, 1 rue Laurent Fries, 67404, Illkirch ,","place":["France"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nadia","family":"Messaddeq","sequence":"additional","affiliation":[{"name":"Institute of Genetics and Molecular and Cellular Biology (IGBMC), INSERM U1258, CNRS UMR7104, University of Strasbourg , 1 rue Laurent Fries, 67404, 1 rue Laurent Fries, 67404, Illkirch ,","place":["France"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chadia","family":"Nahy","sequence":"additional","affiliation":[{"name":"Institute of Genetics and Molecular and Cellular Biology 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