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. 2022 Feb 8;13(2):123. doi: 10.1038/s41419-022-04595-1

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© The Author(s) 2022

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. 7 — The targeted androgens-AR and collagen-integrin α2β1 in PDCs can increase the formation of AR/ARA55/FAK complex that resulted promote the PDCs migration via activation of signaling mediated by ECM–integrin interactions, an effect that translates into increased periosteal bone formation and improved bone fracture repair. AR androgen receptor, ARA55 AR-associated protein 55, FAK focal adhesion kinase, ECM extracellular matrix, PDCs periosteum-derived progenitor cells.