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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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Opa1 overexpression attenuates oxidative stress and improves mitochondrial respiration in hypoxia-treated cardiomyocytes. (A,B) Analysis of mitochondrial ROS production by DHE staining. (C–F) ELISA analysis of manganese superoxide dismutase (MnSOD), glutathione reductase (GR), thioredoxin reductase (TrxR), and peroxiredoxin (PRx) levels in (culture media from) hypoxia-treated cardiomyocytes. (G) Determination of mitochondrial oxygen consumption rate (OCR). (H) Measurement of ATP production in cardiomyocytes subjected to hypoxic stress. (I,J) ELISA/Colorimetric analysis of mitochondrial respiratory complex I and III activities in hypoxia-treated cardiomyocytes. ^∗p < 0.05.

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