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. 2023 Nov 1;55(11):2417–2432. doi: 10.1038/s12276-023-01112-y

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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 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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Fig. 8 — Multiomics analysis of the mouse hippocampus demonstrated that endogenous fructose metabolism was increased in T2DM animals. Further experiments illustrate that endogenous fructose metabolism occurs predominantly in microglia of the hippocampus and is boosted during T2 diabetes mellitus, leading to the overexpression and mitochondrial translocation of NOX4. Translocated NOX4 injures mitochondria and consequently destroys microglial redox hemostasis. Overproduction of ROS from microglia mediates synaptic deficits and promotes the development of DACD. Knocking down Khk downregulates NOX4 expression and mitochondrial translocation and reduces ROS generation in microglia, which in turn restores synaptic impairment and alleviates DACD.