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. 2018 Oct 15;8:15226. doi: 10.1038/s41598-018-33149-9

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© The Author(s) 2018

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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Proposed mechanism for the role of H₂S on HHcy induced bone loss in CBS^+/− mice. First, the HHcy condition is induced in CBS^+/− mice by an alteration of CBS enzyme activity and decreased H₂S production. Second, the HHcy condition further inhibits HDAC activity through oxidative stress. However, administration of NaHS (H₂S donor) or specific HDAC activator (ITSA-1) reverses these effects in CBS^+/− mice. Third, inhibition of HDAC3 further epigenetically regulates histone acetylation and inflammatory gene expression. Fourth, exaggerated inflammatory cytokines expression enhances osteoclastogenesis and bone loss. Fifth, HHcy mediated decreased RunX2 sulfhydration, is reversed by NaHS, thereby bone homeostasis is maintained.