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. 2021 Aug 23;12:474. doi: 10.1186/s13287-021-02526-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. 2 — GnRH, TGF-β, and SHH affect the multiple functions of eMSCs, such as proliferation, differentiation, aging, and migration. GnRH inhibits the multiple beneficial functions of eMSCs, such as proliferation, differentiation, and migration, through the PI3K/AKT signaling. The activation of Akt signaling attenuates the GnRH-induced adverse effects on multiple stem cell functions. TGF-β inhibits the proliferation, differentiation, and colony-forming efficiency of SUSD2⁺ eMSCs. A83-01, TGF-β receptor inhibitor, can maintain the clonogenicity of SUSD2⁺ eMSCs, promote proliferation, prevent cell apoptosis, and maintain eMSC function. Exogenous SHH therapy could significantly alleviate various aging-related declines in multiple eMSC functions through the inhibition of SERPINB2 expression