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. 2018 Apr 4;9:296. doi: 10.3389/fphys.2018.00296

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Copyright © 2018 Yan, Zhang, Wei, Yan, Pan, Yu, Fan, Liu, Zhou, Han and Yao.

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 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 schematic showing the effect and signaling of GLXB on myocardial I/R injury. I/R activates RhoA/ROCK1 signaling that downregulates the expression of ATP 5D, leading to a decrease of ATP production, disintegrating of F-actin and cardiomyocyte necrosis. which contribute to the decrease in myocardial blood flow, myocardium infarct, and heart dysfunction. In addition, ischemia causes lack of oxygen and glucose which exaggerate the dysfunction of mitochondria respiratory chain, leading to oxidative stress and apoptosis, contributing to myocardium infarct, and heart dysfunction. GLXB inhibits RhoA/ROCK1 signaling, attenuates mitochondria dysfunction, thus improves the outcome of animals exposed to I/R.