{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T15:06:16Z","timestamp":1792249576486,"version":"4.4.0"},"reference-count":56,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2018,4,13]],"date-time":"2018-04-13T00:00:00Z","timestamp":1523577600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100009619","name":"Japan Agency for Medical Research and Development","doi-asserted-by":"publisher","award":["16bm0704010h0001"],"award-info":[{"award-number":["16bm0704010h0001"]}],"id":[{"id":"10.13039\/100009619","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2018,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Muscle mitochondria are crucial for systemic metabolic function, yet their regulation remains unclear. The zinc finger MYND domain\u2010containing protein 17 (Zmynd17) was recently identified as a muscle\u2010specific gene in mammals. Here, we investigated the role of Zmynd17 in mice. We found Zmynd17 predominantly expressed in skeletal muscle, especially in fast glycolytic muscle. Genetic\n                    <jats:italic>Zmynd17<\/jats:italic>\n                    inactivation led to morphologic and functional abnormalities in muscle mitochondria, resulting in decreased respiratory function. Metabolic stress induced by a high\u2010fat diet upregulated Zmynd17 expression and further exacerbated muscle mitochondrial morphology in\n                    <jats:italic>Zmynd17<\/jats:italic>\n                    \u2010deficient mice. Strikingly, Zmynd17 deficiency significantly aggravated metabolic stress\u2010induced hepatic steatosis, glucose intolerance, and insulin resistance. Furthermore, middle\u2010aged mice lacking Zmynd17 exhibited impaired aerobic exercise performance, glucose intolerance, and insulin resistance. Thus, our results indicate that Zmynd17 is a metabolic stress\u2010inducible factor that maintains muscle mitochondrial integrity, with its deficiency profoundly affecting whole\u2010body glucose metabolism.\u2014Fujita, R., Yoshioka, K., Seko, D., Suematsu, T., Mitsuhashi, S., Senoo, N., Miura, S., Nishino, I., Ono, Y. Zmynd17 controls muscle mitochondrial quality and whole\u2010body metabolism. FASEB J. 32, 5012\u20135025 (2018).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.201701264r","type":"journal-article","created":{"date-parts":[[2018,4,25]],"date-time":"2018-04-25T16:01:06Z","timestamp":1524672066000},"page":"5012-5025","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":31,"title":["Zmynd17 controls muscle mitochondrial quality and whole\u2010body metabolism"],"prefix":"10.1096","volume":"32","author":[{"given":"Ryo","family":"Fujita","sequence":"first","affiliation":[{"name":"Musculoskeletal Molecular Biology Research Group Basic and Translational Research Center for Hard Tissue Disease Nagasaki University Graduate School of Biomedical Sciences Nagasaki Japan"},{"name":"Department of Stem Cell Biology Nagasaki University Graduate School of Biomedical 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