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. 2022 Apr 4;8:161. doi: 10.1038/s41420-022-00967-w

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© The Author(s) 2022

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 — ATP6AP2, maintaining lysosomal acidification function. When ATP6AP2 was knockdown, cardiomyocyte autophagic flux and mitophagy were blocked. Further leads to the accumulation of dysfunctional mitochondria, increasing reactive oxygen species (ROS), or mitochondrial ROS. Meanwhile, accumulated ROS activates the NLRP3 inflammasome and leads to heart failure. Promoting autophagosome formation via Rapamycin increase NLRP3 activation in shR-ATP6AP2-transfected cardiomyocytes. Conversely, slowing autophagy initiation by 3-MA partially reduces ROS and activation of NLRP3 in shR-ATP6AP2-transfected cardiomyocytes. Green solid arrows show the normal autophagic flux. Arrows in dotted orange indicate that knockdown of ATP6AP2 gene blocks autophagic flux, accumulated undigested mitochondria trigger ROS and NLRP3.