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. 2023 Jul 22;21:494. doi: 10.1186/s12967-023-04246-9

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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. 7 — Schematic illustration of the underlying mechanism of SIRT3 (Sirtuin 3) in regulating MAM coupling. Under normal conditions, SIRT3 is highly expressed and promotes VDAC1 deacetylation. Hypoacetylated VDAC1 binds to cytoplasmic chaperone GRP75 and tethers ER-resident inositol IP3R with low affinity. During hyperglycemia, SIRT3 expression is inhibited, leaving VDAC1 in a hyperacetylated state. Hyperacetylated VDAC1 displays significantly stronger interaction with GRP75 and IP3R, resulting in increased MAM formation, mitochondrial dysfunction and apoptosis