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. 2020 Aug 28;8:853. doi: 10.3389/fcell.2020.00853

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Copyright © 2020 Xin, Lv, Liu, Jing and Hu.

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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Overexpression of Opa1 attenuates cardiac damage and dysfunction induced by hypoxic stress. (A–C) ELISA analysis of troponin T (TnT), troponin I (TnI), and creatine kinase MB (CK-MB) secretion by Opa1-overexpressing (Ad-Opa1) and Opa1-knockdown (si-Opa1) cardiomyocytes subjected to 24 h hypoxia exposure. (D,E) Analysis of cardiomyocyte contractile properties. Maximal shortening and relengthening velocities were measured using a SoftEdge MyoCam system. (F,G) Myosin immunofluorescence results. ^∗p < 0.05.