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. 2022 May 14;20:222. doi: 10.1186/s12967-022-03408-5

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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. 2 — CSE-induced mitochondrial oxidative stress dysregulated lipid metabolism to activate LF. A Nile Red staining was performed to show lipid content in cells treated as indicated. B The effect of CSE on protein level of CPT1a and PPARα which were related with FAO. C The effect of PPARα activator Feno on CPT1a level. D Western blot to determine the level of Collagen I and α-SMA. E The role of MitoQ in CPT1a and PPARα expression. F Nile Red staining. G Western blot analysis for Collagen I and α-SMA expression. *p < 0.05 versus control, ^#p < 0.05 versus CSE, ^&p < 0.05 versus CSE + Feno or CSE + MitoQ. Feno fenofibrate, ETO etomoxir, OA oleic acid