Rheumatoid arthritis (RA), an autoimmune condition that has a significant inflammatory component and is exacerbated by dysregulated redox-dependent signaling pathways. In RA, the corelationship between oxidative stress and inflammation appears to be regulated by the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway. Furthermore, it has been shown that transcriptional pathways involving Nrf2 and NFκB significantly interact under conditions of oxidative stress and inflammation. Because pathologic cells in RA have a higher chance of surviving, Nrf2's influence on concomitant pathologic mechanisms in the disease is explained by its interaction with key redox-sensitive inflammatory pathways. The current review not only updates knowledge about Nrf2's function in RA but also highlights the complex interactions between Nrf2 and other redox-sensitive transcription factors, which are essential to the self-sustaining inflammatory processes that define RA. This paper also reviews the candidates for treating RA through Nrf2 activation. Finally, future directions for pharmacologic Nrf2 activation in RA are suggested.
© 2024 The Author. Published by American Chemical Society.