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. 2023 Jan 10;21:16. doi: 10.1186/s12967-023-03873-6

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© The Author(s) 2023

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. 4 — Post-MI mediated cardiac mitochondrial ROS over-production, membrane depolarization and mitochondrial swelling. Post-MI increased mitochondrial fission and reduced mitochondrial fusion. Quantitative analysis of: A Mitochondrial ROS production; B Mitochondrial membrane potential; C Mitochondrial swelling; D cardiac tissue pDRP1/tDRP1; E cardiac tissue MFN1/GAPDH; F cardiac tissue MFN2/GAPDH; G cardiac tissue OPA1/GAPDH; n = 5–6 per group. All bar charts are expressed as mean ± SEM. *p < 0.05 vs. SHAM. MI myocardial infarction; ROS reactive oxygen species