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. 2021 Oct 30;12:557. doi: 10.1186/s13287-021-02623-z

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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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — A summary diagram that leptin promotes megalin expression mediated by inhibition of CMA and synergistically with 25(OH)D₃ to promote the osteoblast differentiation of rBMMSCs. As indicated by these studies, leptin inhibited the activity of CMA by activating PI3K/AKT signaling pathway to promote the expression of megalin, and then the quantity of 25(OH)D₃ entering rBMMSCs was increased through increased megalin receptors. 25(OH)D₃ was converted to 1α,25(OH)₂D₃ by 1α-hydroxylation of mitochondrial CYP27B1, and the synthesis of 1α,25(OH)₂D₃ was up-regulation and stimulated osteoblast differentiation of rBMMSCs