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. 2022 Aug 16;11(11):598–621. doi: 10.1089/wound.2021.0065

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© Norifumi Urao et al., 2022; Published by Mary Ann Liebert, Inc., publishers

This Open Access article is distributed under the terms of the Creative Commons License [CC-BY] (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 3. — The chronic signals of HSPCs under conditions with chronic inflammation. TLR4, IL-1, and IL-6 are important mediators in chronic signal pathways. They utilize the same downstream pathway to activate myeloid skewing. ROS are produced from mitochondria in reaction to chronic inflammation. ROS dysregulates HSPC function by upregulating the specific transcription factors such as FoxO and Gfi1. p38 MAPK pathway is also activated by ROS resulting in the inhibition of HSPC self-renewal. The sympathetic nerve system plays an essential role in HSPC differentiation as a part of the bone marrow niche. TGF-β is produced from glial cells ensheathing sympathetic nerves and negatively regulates HSPC proliferation. TGF-β noncanonical pathway (dashed line) has crosstalk with other signaling pathways to orchestrate HSPC function. FoxO, forkhead box O; Gfi1, growth factor independent 1 transcription repressor; MAPK, mitogen-activated protein kinase; ROS, reactive oxygen species; TGF-β, transforming growth factor-beta.