Saha Sarmistha
Department of Biotechnology, Institute of Applied Sciences & Humanities, GLA University, Mathura 281406, Uttar Pradesh, India.
ACS Omega. 2024 Feb 20;9(9):10049-10057. doi: 10.1021/acsomega.4c00163. eCollection 2024 Mar 5.
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.
类风湿性关节炎（RA）是一种自身免疫性疾病，具有显著的炎症成分，且因氧化还原依赖性信号通路失调而加剧。在类风湿性关节炎中，氧化应激与炎症之间的相互关系似乎受核因子红细胞2相关因子2（Nrf2）信号通路调控。此外，研究表明，涉及Nrf2和NFκB的转录途径在氧化应激和炎症条件下会显著相互作用。由于类风湿性关节炎中的病理细胞存活几率更高，Nrf2对该疾病伴随病理机制的影响可通过其与关键氧化还原敏感炎症途径的相互作用来解释。本综述不仅更新了关于Nrf2在类风湿性关节炎中功能的知识，还强调了Nrf2与其他氧化还原敏感转录因子之间的复杂相互作用，这些相互作用对于定义类风湿性关节炎的自我维持炎症过程至关重要。本文还综述了通过激活Nrf2治疗类风湿性关节炎的候选药物。最后，提出了类风湿性关节炎中Nrf2药理激活的未来研究方向。
