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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. 2 — LSCs have a remodeling effect of the BM niche by multiple pathways, such as activating the production of abnormal osteoblastic lineage cells from mesenchymal progenitor cells (MPCs). The interaction between LSCs and MSCs, including the transfer of ROS and mitochondria, is conducive to maintaining a low intracellular ROS level and energy metabolism of LSCs under a hypoxic environment. In addition, it has been indicated that 1. hematopoietic stem cell-supporting and retention factors secreted by bone marrow matrix cells, such as SCF and CXCL12 etc., have an important role in HSCs maintenance; 2. exosomes derived from leukemic cells may interfere and destroy HSCs maintenance by downregulating SCF and CXCL12.; 3 HSCs mobilization in bone marrow niche is accelerated; 4. In the pro-oxidative treatment, LSCs can respond by upregulating antioxidant, MCL-1, MPO, and HO-1. As leukemia is a highly heterogeneous disease, the survival and redox regulation mechanisms of LSCs in the BM niche may vary for different types of leukemia. More studies are needed for revelation in this subject.