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In amyloid precursor protein plus presenilin-1 (APP/PS1) mice, Nrf2 overexpression caused by antioxidant therapy has been demonstrated to improve neuronal apoptosis, increase thioredoxin-1 (TRX-1), and prevent the formation of NLRP3 inflammatory bodies [109]

The p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK) MAPK signaling pathways were activated by the S

Glutathione can be produced by the body and is typically concentrated within the liver

Because inflammation is a core component and driver of NASH pathology, the anti-inflammatory actions of FGF21-based therapies are likely to benefit the general NASH patient population