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. 2023 Mar 28;19(5):1177–1184. doi: 10.1007/s12015-023-10533-1

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© The Author(s) 2023

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/.

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Fig. 1 — The novel role of Nox2-ROS-Nlrp3 inflammasome axis in regulating the biology of HSPCs. Intracellular ROS in HSPCs is generated by hematopoietic cells specific Nox-2 in response to stimulation by peripheral blood-derived C3a or C5a activating C3aR and C5aR on the outer cell membrane (A), and C5aR expressed on mitochondria membrane by complosome-derived intracellular C5a (B). Subsequently, generated in cytosol ROS activate Nlrp3 inflammasome that releases several DAMPs or alarmin including IL-1β1, S100A8/A9, HMGB-1 and eATP that interact with corresponding receptors on cell surface to produce more ROS to further augment Nlrp3 inflammasome activation (C). These signals within non-toxic to the cell “hormetic zone of activation” [23, 24] enhance metabolism and migration of HSPCs