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. 2019 Dec 6;4:56. doi: 10.1038/s41392-019-0094-1

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© The Author(s) 2019

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. 5 — a–g Immunoblotting assay for mitophagy markers. FUNDC1 siRNA was used to knockdown the expression of FUNDC1. h–j Costaining of mitochondria and lysosomes. Mitochondria were labeled with Tom-20, and lysosomes were labeled via LAMP1. Organ immunofluorescence was the hallmark of the interaction between mitochondria and lysosomes, which was indicative of mitophagy. FUNDC1 siRNA was used to knockdown the expression of FUNDC1. The mitochondrial length was evaluated to reflect mitochondrial fission. k ATP production in primary hepatocytes with DNA-PKcs deletion or FUNDC1 knockdown under alcohol treatment. l–p Effects of mitophagy on state 3 respiration, state 4 respiration, the respiratory control ratio (RCR [state 3/state 4]), number of nmol of ADP phosphorylated to atoms of oxygen consumed (ADP/O), and the ADP phosphorylation lag phase (time elapsed in the depolarization/repolarization cycle during ADP phosphorylation). The experiments were repeated three times with similar results. The data represent the mean ± standard error of the mean. *p < 0.05.