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. 2021 Aug 3;12:717187. doi: 10.3389/fphys.2021.717187

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Copyright © 2021 Cheng, Zheng, Hu, Lv and Lu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Silencing of Fis1 or BAP31 attenuates mitochondrial division and oxidative stress. (A–C) Cardiomyocytes were subjected to hypoxia to mimic myocardial infarction in vitro. SiRNAs were used to attenuate Fis1 or BAP31 expression in cardiomyocytes. Then, an immunofluorescence assay was used to detect the mitochondrial morphology. The average length of the mitochondria and the percentage of fragmented mitochondria were recorded. (D,E) MtROS were detected using an immunofluorescence assay. (F,G) ELISAs were used to analyze anti-oxidative enzyme activity. *p < 0.05.