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In addition, the Mst1/Hippo, RAGE/NF-B, ROS/NF-B, TLR4/MyD88/MAPKS/NF-B, and SIRT1/FOXO3a/MnSOD signaling pathways are also found to be involved in ISO-induced oxidative stress injury in the heart (139, 165168)

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In vitro, it was reported that the spontaneous electrophilic attack of the FA carbonyl group to the thiol-group of GSH leads to the formation of the covalent product S-hydroxymethyl-GSH (HSMGSH) 15

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Furthermore, GPx1-deficient hearts had decreased cardiac contractility and worse diastolic dysfunction in response to doxorubicin compared to wild type hearts [43]