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. Author manuscript; available in PMC: 2021 Nov 25.
Published in final edited form as: Neuron. 2020 Sep 7;108(4):608–622. doi: 10.1016/j.neuron.2020.08.012

Figure 3. Pro-inflammatory cytokine-induced epigenetic suppression of NRF2 signaling during CNS inflammation.

Figure 3.

During initial exposure to inflammatory signals, astrocytes upregulate the formation of MAFG homodimers, which outcompete MAFG/NRF2 heterodimer binding to transcriptional response elements that control NRF2 signaling. In addition, MAT2α cooperates with MAFG and induces DNA methylation marks that restrict chromatin accessibility. Collectively, these epigenetic modifications suppress NRF2-driven inhibition of NF-κB signaling and lead to sustained inflammation.