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This study showed that inhibiting HMGB1 nucleocytoplasmic translocation pharmacologically and deleting HMGB1 in TECs in mice were effective in preventing IRI-AKI, tubular ferroptosis, and inflammation compared to control groups [48]

This might be associated with the high hydrophilicity of these substances

Corrector therapies (with or without potentiators) for people with cystic fibrosis with class II CFTR gene variants (most commonly F508del)

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Although exogenous factors, including infection and inhaled pollutants, could directly oxidize GSH, endogenous disease-specific mechanisms could also prime the process