Research Article

Protection against HEMA-Induced Mitochondrial Injury In Vitro by Nrf2 Activation

Figure 7

Proposed mechanisms for protection by Nrf2 against HEMA-induced cellular toxicity. Under physiological conditions, Nrf2 is sequestered in the cytosol and maintained at a low level through Keap1-mediated degradation. Resin monomers like HEMA disturb Keap1-mediated degradation of Nrf2 by increased oxidative stress and GSH depletion and/or by direct reaction with thiol groups of Keap1, to activate the Nrf2 pathway. Nrf2 neutralizes ROS and regenerates GSH, thus reducing ROS-mediated apoptosis and mitochondrial damage; Nrf2 restores impaired mitochondria by regulating the PGC1α/NRF1 pathway.