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. 2021 Jun 28;12:653349. doi: 10.3389/fphys.2021.653349

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Copyright © 2021 Wei, Guo, Pan, Li, Cui, Yan, Fan, Deng, Hu, Chang, He, Yan, Sun, Wang and Han.

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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A diagrammatic sketch showing the pathways that lead to the protected effects of T₈₉ on ISO-induced cardiac injury. ISO causes enhancement of glycolysis and reduction of fatty acid metabolism and oxidative phosphorylation, resulting in energy disorder and oxidative stress with myocardial injury and reduction of MBF. Meanwhile, ISO-educed cardiac hypertrophy via regulating HSP70-ERK1/2 signals, which, together with cardiac injury, finally caused reduction of heart function and low survival rate. Nevertheless, T₈₉ administration reversed all the above alteration. The cardioprotective role of T₈₉ depended on the regulation of glycolipid metabolism, recovery of mitochondrial function, and improvement of myocardial energy.