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. 2022 Dec 19;12:204. doi: 10.1186/s13578-022-00935-y

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© The Author(s) 2022

Open AccessThis 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 8 — FOXO3a and PARKIN formed regulatory axis of mitophagy and hypertrophy. A and B, FOXO3a inhibited cardiomyocyte hypertrophy through targeting PARKIN. After being infected with FOXO3a adenovirus, cardiomyocytes were infected with PARKIN siRNA or PARKIN scramble, and then treated with Ang II. A Cell surface area indicated by phalloidin-TRITC conjugate stained F-actin were calculated. * p < 0.05. ** p < 0.01. n = 3 experiments per group. B The mRNA levels of ANP and BNP were detected. * p < 0.05. n = 3 experiments per group. C, FOXO3a regulated mitophagy through targeting PARKIN. After being infected with FOXO3a adenovirus, cardiomyocytes were infected with PARKIN siRNA or PARKIN scramble, and then treated with Ang II. Immunoblot were performed to detect protein levels of LC3I and LC3II. The ratio of LC3II/LC3I was calculated. ** p < 0.01. n = 3 experiments per group