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. 2020 Apr 27;11(4):291. doi: 10.1038/s41419-020-2488-y

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© The Author(s) 2020

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. 1 — The ROS level of HSCs in quiescence is regulated by a complex signaling network consisting of ATM, HIFs, FoxOs, SRC3, etc., which work together to maintain a low intracellular ROS level. The interaction between HSCs and BMSCs in the BM niche has a vital role in the long-term stability of HSCs. TPO, SCF, TGF-β1, and BMPs produced by BMSCs are all important regulators of the quiescence of HSCs.