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Transgenic mice in which GCLC expression is abolished in hepatocytes have 58% of normal hepatic GSH levels and manifest liver pathologies characteristic of the various clinical stages of fatty liver disease 8,9

DAlessandro A et al (2023e) Metabolic signatures of cardiorenal dysfunction in plasma from sickle cell patients as a function of therapeutic transfusion and hydroxyurea treatment

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GSTs have emerged as a promising therapeutic target because specific isozymes are overexpressed in a wide variety of tumors and may play a role in the etiology of other diseases, including neurodegenerative diseases, multiple sclerosis, and asthma