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. 2021 Apr 25;473(6):969–976. doi: 10.1007/s00424-021-02561-y

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — Schematic illustration of myostatin-induced FGF23 production in UMR106 cells. Myostatin binding to ACVR2B and following partnering with TGF-βRI activates p38MAPK and NFκB. NFκB induces SOCE, resulting in induction of Fgf23 gene expression. Created with BioRender.com. Activin type 2 receptor B (ACVR2B); fibroblast growth factor 23 (FGF23); nuclear factor kappa-light-chain-enhancer of activated B-cells (NFκB); p38 mitogen–activated protein kinase (p38MAPK); store-operated Ca^2 + entry (SOCE); transforming growth factor-β type I receptor (TGF-βRI)