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. 2023 Jan 18;11:7. doi: 10.1038/s41413-022-00241-w

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© The Author(s) 2023

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — The role of osteocyte Phd2 in vivo. Wild type (WT) male mice were fed an adenine diet (AD) to induce CKD for 2, 4, or 6 weeks. Mice on casein diet for 8 weeks were used as controls. a Bone Fgf23 (blue) and Egln1/Phd2 (red) mRNA expression was measured over diet duration. b Male Phd1 and c Phd3 expression in CKD bone. Numbers above timepoints indicate the % decrease in gene expression compared to the casein diet control (n = 3–4 mice/group; **P < 0.01; ***P < 0.001 vs. casein diet control). Fgf23 mRNA expression in d whole bone (including marrow), e osteocyte-enriched bone fractions, and f plasma total (C-terminal) FGF23 concentrations in mice with conditional deletion of Phd2 in osteocytes (Phd2-fl/fl/Dmp1-cre⁺) compared to mice without deletion (Phd2-fl/fl/Dmp1-cre⁻) (n = 6 mice/genotype; *P < 0.05, ***P < 0.001 vs. cre⁻ mice)