Activation of Nrf2/AREs-mediated antioxidant signalling, and suppression of profibrotic TGF-β1/Smad3 pathway: a promising therapeutic strategy for hepatic fibrosis — A review

Activation of the Nrf2-AREs pathway may serve as a novel therapeutic target for hepatic fibrosis.

• Hepatic fibrosis is characterized by excessive buildup of extracellular matrix components due to chronic liver injury.
• Hepatic stellate cell activation is a major driver of this excessive extracellular matrix production.
• Transforming growth factor-β1 (TGF-β1) stimulates both hepatic stellate cell activation and excessive extracellular matrix accumulation.
• Oxidative stress is implicated as a key event in the development of liver fibrosis.
• The Nrf2-AREs pathway is associated with the activation of detoxifying enzymes and antioxidant responses.
• Recent findings suggest that targeting the Nrf2-AREs pathway may help suppress the profibrotic TGF-β1/Smad3 pathway.

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