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. 2023 Nov 25;28:540. doi: 10.1186/s40001-023-01520-w

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© The Author(s) 2023

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/. 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. 5 — ATF6 increase Sirt1 sulfhydration by promoting H₂S production through upregulating CBS expression. ATF6 binds to the promotor region of CBS, a vital H₂S producing enzyme in the liver, and promote the protein transcription. The upregulation of CBS enhances H₂S production. Accumulation of H₂S stimulates Sirt1 sulfhydrylation, then inhibits its downstream SREBP expression, to reduce lipogenesis and fatty acid beta-oxidation. In addition, Sirt1 sulfhydrylation decrease expression of pro-inflammatory factor IL-17A, and increase anti-inflammatory factor IL-10 expression. ATF6 could mitigate the liver lipogenesis and inflammation by stimulating sulfhydrylated Sirt1 through CBS/H₂S pathway