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Thus, this study revises the conventional doctrine of GSH function in protein redox regulation and liver pathophysiology, indicating that hepatic GSH depletion by Chac1 overexpression may represent a potentially novel therapeutic approach for MASLD (Figure 6G)

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Asico L, Zhang X, Jiang J, Cabrera D, Escano CS, Sibley DR, et al

Learn More Research review and sources Primary references and supporting sources Nicotinamide N-methyltransferase inhibition mitigates obesity-related metabolic dysfunction Recent preclinical 5A1MQ paper describing obesity, glucose, and liver endpoints