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. 2019 Nov 19;38:469. doi: 10.1186/s13046-019-1456-9

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 9 — The HCC microenvironment inhibits SIRT4 expression in TAMs and modulates alternative activation of TAMs, which contributes to HCC development. The HCC microenvironment inhibits SIRT4 expression in TAMs. The downregulation of SIRT4 increases FA oxidation and the expression of lipid catabolic genes, which induces alternative activation of TAMs via the FAO-PPARδ-STAT3 signalling pathway. Alternatively activated TAMs produce IL-6 to accelerate HCC development and produce IL-10 to accelerate M1 macrophage apoptosis. On the other hand, downregulation of SIRT4 in hepatocytes activates MCP-1 expression to increase TAM infiltration, which accelerates HCC development via the NF-κB signalling pathway