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. 2022 Aug 17;54(8):1067–1075. doi: 10.1038/s12276-022-00829-6

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© The Author(s) 2022

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Fig. 2 — In unstressed conditions, Keap1 binds to the Cul3-containing E3 ubiquitin ligase complex, and two molecules of Keap1 form a homomeric dimer. The Keap1 complex binds to Nrf2 for the ubiquitination and subsequent degradation of Nrf2 by the proteasome. Under conditions of oxidative stress, Keap1 undergoes a conformational change, which leads to blocked ubiquitination of Nrf2 and accumulation of newly synthesized Nrf2. Subsequently, free Nrf2 is translocated to the nucleus, where it forms a heterodimer with small Maf proteins. Then, Nrf2-Maf interacts with the ARE in the promoter regions of DNA to promote the transcription of multiple targeted antioxidant genes, including HO-1, GSH, SOD, CAT, and NQO1. Activating Nrf2 signaling protects against oxidative stress in disc cells to alleviate IDD.