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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 overexpression sustains mitochondrial homeostasis. Adenovirus loaded with AMPKα2 were transfected into cardiomyocytes before H/R injury. (A,B) Mitochondrial membrane potential was measured through JC-1 probe relative fluorescence intensity in H/R cardiomyocytes. (C,D) Intracellular ROS were determined through immunofluorescence. (E,F) H/R-mediated calcium overload was determined through immunofluorescence. (G,H) ELISA was used to measure the activities of caspase-9 and Bax in cardiomyocytes treated with H/R injury. The data represent the mean ± SEM. P < 0.05.