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. 2022 Dec 26;19:314. doi: 10.1186/s12974-022-02678-6

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© The Author(s) 2022

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. 8 — Mechanism of neuroinflammation regulation by lactate via NDRG2 (N-Myc downstream-regulated gene 2) and TNFα. Phosphorylated c-Jun promotes the expression of TNFα, which exacerbates neuroinflammation and damages neighboring cells. However, lactate directly binds with NDRG2 and inhibits its ubiquitination and degradation. NDRG2 inhibits c-Jun phosphorylation and thus subsequently inhibits TNFα production. This finding suggests a valuable approach for modulating neuroinflammation during the early stages of ischemia (Created with www.BioRender.com)