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Impaired insulin signaling, diminished mitochondrial oxidative capacity, lipid peroxidation, ferroptosis, and microbial dysbiosis not only exacerbate hepatic steatosis but also facilitate the progression from simple steatosis to more severe forms of the disease, such as NASH and cirrhosis [51,56,63,64,65,66,67]
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We hope these assays and insights will be adopted more broadly to build larger datasets of GST substrate preferences, ultimately enabling more predictive frameworks for GST-mediated metabolism, similar to those established for CYP450s
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