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However, during the chronic inflammation, the glial activation causes an increase of ROS production and other neurotoxic mediators, leading a neuronal damage [52]
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One hypothesis is that we observed a greater induction of NRF2 through liver-specific Gclc deletion as compared to KEAP1 inhibition with CDDO-me because CDDO-me is a weaker inhibitor of NRF2-KEAP1 interaction compared to the ROS generated following GSH depletion
PMID: 122 HarleyITWStankiewiczTEGilesDASofticSFlickLMCappellettiMet al
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