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. 2021 Jun 15;12(6):614. doi: 10.1038/s41419-021-03876-5

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© The Author(s) 2021

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. 7 — A The sh-MARCH5 or sh-NC was intraperitoneally administered 24 h before myocardial I/R injury (n = 6). Post-I/R injury, RNA was isolated and the expression of MARCH5 was determined by qRT-PCR and western blot. B, C The left panel shows representative images of heart tissues. The right panels show the infarct size (%), infarct area/left ventricle (INF/LV) and LVIDd (n = 6). D Representative TEM images of heart tissues and quantification of fragmented mitochondria (%) (Scale bar = 0.5 μm) (n = 6). E The levels of ROS, ATP and OCR were measured to evaluate mitochondrial function in H/R-treated cardiomyocytes, which were transfected with sh-MARCH5 or sh-NC. JC-1staining (2ug/ml) was used to analyze mitochondrial membrane potential (△Ψm) (n = 3). **P < 0.01; ***P < 0.001.