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. 2022 Apr 6;5:326. doi: 10.1038/s42003-022-03251-w

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© The Author(s) 2022

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. 7 — GSTM2 was highly up-regulated in hepatic steatosis tissues. As the member of phase II drug metabolizing enzymes, GSTM2 could detoxify the toxicity of metabolic products such as ROS. ROS could enhance the inflammation and fibrosis progression. Furthermore, GSTM2 interacted with ASK1 directly and suppressed ASK1 phosphorylation. Therefore, GSTM2 down-regulated expression of SREBP and perilipins to inhibit the LD accumulation. ASK1 signaling also regulated the expression level of DGAT2, GPAT4 and PCYT1A and the recruitment of DGAT2 and GPAT4 on LD surface to modulate the LD growth. In conclusion, GSTM2 protects against the hepatic steatosis of NAFLD via its antioxidant and suppressing ASK1-p38/JNK signaling.