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. 2020 Aug 27;8:833. doi: 10.3389/fcell.2020.00833

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Copyright © 2020 Deng, Chen, Zhang, Li, He and Tan.

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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AMPK2α sustains mitochondrial dynamics through the Sirt3/PGC1α signaling pathway. (A,B) RNA was isolated from cardiomyocyte, and qPCR was used to evaluate the transcription of Sirt3 and PGC1α. (C–E) Immunofluorescence assay for Sirt3 and PGC1α in cardiomyocytes treated with H/R injury. (F–H) Mitochondrial morphology was determined through immunofluorescence. 3-TYP, an inhibitor of the Sirt3/PGC1α signaling pathway, was added into the cardiomyocyte medium before AMPK2α overexpression. The data represent the mean ± SEM. P < 0.05.