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. 2020 Feb 20;24(4):1573–1580. doi: 10.1007/s11325-020-02029-w

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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 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 — Effect of intermittent hypoxia, oxidative stress, and inflammation on activation of nuclear factor-κB (NF-κB) by stimulation of receptor for advanced glycation end products (RAGE) and Toll-like receptors (TLRs) through extracellular high-mobility group box 1 protein (HMGB1). Nuclear HMGB1 acts as a DNA chaperone with DNA binding and bending activities and regulates replication, recombination, repair, and transcription