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Cardiomyopathy includes fibrosis of cardiac wall tissue at later disease stages with thickening of the left ventricle wall (Hanson et al., 2019)

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This enhanced tolerance could be relevant to the increased transcription of the GSH cycle-related genes and increased GSH content and biosynthesis, and decreased the transcription of Cd transporter genes

Notably, similar inhibitions were observed both with the wild type enzyme and its cysteine mutants, suggesting that thiol conjugation is dispensable for GST inactivation by auronofin in contrast to other described targets 103

Nrf2 transcriptionally activates GGT [29], which plays a key role in glutathione homeostasis by breaking down extracellular glutathione into its constituent parts, which can be taken up by the cell for intracellular glutathione synthesis [30]