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. 2020 Sep 24;10:15711. doi: 10.1038/s41598-020-72594-3

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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 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/.

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A proposed scheme illustrating the potential role of STAT3 phosphorylation on Ser727 in regulating mitochondrial autophagy. While P-STAT3^Tyr705 localized in the nucleus of H. pylori infected AGS cells transactivates the target genes, STAT3 phosphorylated on Ser727 is imported into mitochondria by interacting with GRIM-19. P-STAT3^S727 localized in mitochondria may direct autophagosome formation through an unknown mechanism. Autophagic clearance of impaired mitochondria can maintain tissue homeostasis or cause inflammation, depending on the extent of mitochondrial autophagy.