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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. 8 — The activated DNA-PKcs/p53 pathway enhanced Drp1 transcription and migration to the mitochondria, inducing mitochondrial fission. Meanwhile, p53 also increased the expression of CK2, impairing FUNDC1-required mitophagy via the phosphorylation of FUNDC1 at Ser13. The excessive fission and badly structured mitophagy were associated with mitochondrial dysfunction, leading to hepatic apoptosis and the progression of ARLD.