Involvement of Nrf2 in Ocular Diseases

Figure 1

Proposed molecular mechanisms of oxidative stress-induced Nrf2 activation. Under nonstressed conditions, Keap1 keeps Nrf2 sequestered in the cytosol, where it mediates proteasomal degradation of Nrf2. Under oxidative-stressed conditions, cysteine residues of Keap1 are oxidized, forming a disulfide bridge. Oxidized Keap1 dissociates from Nrf2, allowing Nrf2 to translocate to the nucleus, bind to the ARE region, and initiate transcription of target genes.