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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. 5 — The protective effect of SIRT1 was mediated by mitochondrial redox balance. A Level of SOD2 and mtNOX4. B mtROS level were examined by mitoSOX indicator. C Autophagosomes (yellow) and autolysosomes (red) were evaluated. D SOD2 were knocked down by siRNA, followed by CSE and SRT1720 treatment. Then, p62, LC3 I and LC3 II expression was determined. E–F LC3 (E) and lysosome (F) and LDs were stained to show lipophagy. G Cellular lipid content was evaluated by Nile Red staining. H Expression of collagen I, α-SMA, CPT1a and PPARα. *p < 0.05 versus control, ^#p < 0.05 versus CSE, ^&p < 0.05 versus CSE + SRT1720 (n = 3)