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. 2022 Jan 10;13:4. doi: 10.1186/s13287-021-02677-z

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© The Author(s) 2021

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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 7 — Illustration of mechanisms that HMGB1 modification improves the mobility of mesenchymal stem cells. HMGB1 activates cAMP/PKA to stabilize β-catenin by phosphorylation of GSK3β and β-catenin at Ser675, enabling β-catenin to accumulate intracellularly and translocate into the nucleus. The CTH promoter is thereafter activated by interaction of β-catenin with TCF/LEF, stimulating gene transcription. Cytoplasmic CTH catalyzes endogenous production of hydrogen sulfide from organic sulfide substrates like cystathionine. The Cav 3.2 T-type calcium channel is activated by hydrogen sulfide to drive extracellular calcium influx, and calcium signaling pathway is subsequently activated to promote cell mobility. Besides, HMGB1 presumably interacts with CTH to inhibit the catalysis of hydrogen sulfide production when it is oxidized by oxidative stress