Fibroblast growth factor 23 induces myogenic differentiation of mouse muscle satellite cells in an FGF receptor 4 dependent manner

Abstract

Abstract Fibroblast growth factor 23 (FGF23) is known for regulating phosphate and vitamin D metabolism, but its function in muscle satellite cells and skeletal muscle is unclear yet. Our study explores the role of muscle satellite cells and FGF23 in muscle development, and we specifically investigated the FGF23/FGFR4 signaling pathway in muscle satellite cells and its effect on myogenic differentiation, which is essential for the treatment of skeletal sarcopenia. We treated male C57BL/6J mice with hydrocortisone and d-galactose to establish a model of skeletal sarcopenia to observe the expression of FGF23, FGFR4, and other related proteins. The expression of myosin heavy chain (MHC), myogenic fiber differentiation (MyoD) and FGFR4 was up-regulated after transfection of muscle satellite cells with FGF23 overexpression vector and down-regulated after transfection of muscle satellite cells with FGF23 siRNA.The expression levels of MHC and MyoD were higher than those of the empty vector group after transfection of FGF23 siRNA and FGFR4 overexpression vector.Our findings suggest that FGF23 is a novel factor in regulating skeletal muscle mass, and the FGF23/FGFR4 signaling pathway plays a crucial role in the myogenic differentiation of muscle satellite cells. This finding offers a new potential therapeutic approach for the treatment of sarcopenia.