{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,14]],"date-time":"2026-08-14T18:51:41Z","timestamp":1786733501494,"version":"build-2736575974"},"reference-count":59,"publisher":"American Physiological Society","issue":"4","funder":[{"DOI":"10.13039\/100000049","name":"HHS | NIH | National Institute on Aging (U.S. National Institute on Aging)","doi-asserted-by":"publisher","award":["P01AG039355"],"award-info":[{"award-number":["P01AG039355"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["R01AR070175"],"award-info":[{"award-number":["R01AR070175"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["1K08DK110429"],"award-info":[{"award-number":["1K08DK110429"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"name":"VA Merit Award","award":["BX001471"],"award-info":[{"award-number":["BX001471"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Endocrinology and Metabolism"],"published-print":{"date-parts":[[2018,10,1]]},"abstract":"<jats:p> Skeletal muscle dysfunction accompanies the clinical disorders of chronic kidney disease (CKD) and hereditary hypophosphatemic rickets. In both disorders, fibroblast growth factor 23 (FGF23), a bone-derived hormone regulating phosphate and vitamin D metabolism, becomes chronically elevated. FGF23 has been shown to play a direct role in cardiac muscle dysfunction; however, it is unknown whether FGF23 signaling can also directly induce skeletal muscle dysfunction. We found expression of potential FGF23 receptors ( Fgfr1\u20134) and \u03b1-Klotho in muscles of two animal models (CD-1 and Cy\/+ rat, a naturally occurring rat model of chronic kidney disease-mineral bone disorder) as well as C<jats:sub>2<\/jats:sub>C<jats:sub>12<\/jats:sub> myoblasts and myotubes. C<jats:sub>2<\/jats:sub>C<jats:sub>12<\/jats:sub> proliferation, myogenic gene expression, oxidative stress marker 8-OHdG, intracellular Ca<jats:sup>2+<\/jats:sup> ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>), and ex vivo contractility of extensor digitorum longus (EDL) or soleus muscles were assessed after treatment with various amounts of FGF23. FGF23 (2\u2013100 ng\/ml) did not alter C<jats:sub>2<\/jats:sub>C<jats:sub>12<\/jats:sub> proliferation, expression of myogenic genes, or oxidative stress after 24- to 72-h treatment. Acute or prolonged FGF23 treatment up to 6 days did not alter C<jats:sub>2<\/jats:sub>C<jats:sub>12<\/jats:sub> [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> handling, nor did acute treatment with FGF23 (9\u2013100 ng\/ml) affect EDL and soleus muscle contractility. In conclusion, although skeletal muscles express the receptors involved in FGF23-mediated signaling, in vitro FGF23 treatments failed to directly alter skeletal muscle development or function under the conditions tested. We hypothesize that other endogenous substances may be required to act in concert with FGF23 or apart from FGF23 to promote muscle dysfunction in hereditary hypophosphatemic rickets and CKD. <\/jats:p>","DOI":"10.1152\/ajpendo.00343.2017","type":"journal-article","created":{"date-parts":[[2018,3,20]],"date-time":"2018-03-20T15:15:10Z","timestamp":1521558910000},"page":"E594-E604","source":"Crossref","is-referenced-by-count":41,"title":["Fibroblast growth factor 23 does not directly influence skeletal muscle cell proliferation and differentiation or ex vivo muscle contractility"],"prefix":"10.1152","volume":"315","author":[{"given":"Keith G.","family":"Avin","sequence":"first","affiliation":[{"name":"Department of Physical Therapy, School of Health and Rehabilitation Sciences, Indiana University, Indianapolis, Indiana"},{"name":"Division of Nephrology, Department of Medicine, Indiana University School of Medicine, Indianapolis, 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