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. 2020 Nov 6;11(11):953. doi: 10.1038/s41419-020-03160-y

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© The Author(s) 2020

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. 1 — p66Shc silencing was induced via lentiviruses delivered to C57BL/6 mice exposed to APAP (300 mg/kg). a, b Liver p66Shc, p52Shc, and p46Shc protein, n = 3. ^**p < 0.01 vs. the control group. c Serum ALT levels, n = 8. d Serum AST levels, n = 8. e H&E staining. Scale bar, 200 μm. f, g Mitochondrial dynamics perturbation was determined via TEM (×2000/×10,000, magnification, red arrow). h Liver H₂O₂ levels, n = 8. i Liver GSH levels, n = 8. j Liver MDA levels, n = 8. k, l Liver p66Shc, p-p66Shc, OMA1, L-OPA1, S-OPA1, MFN2, DRP1, p-DRP1 protein, n = 3. m, n Liver OMA1 ubiquitination level, n = 3. ^*p < 0.05, ^**p < 0.01 vs. the LV-control group; ^#p < 0.05, ^##p < 0.01 vs. the APAP group.