Liu Lu, de Leeuw Karina, van Goor Harry, Westra Johanna
Department of Rheumatology and Clinical Immunology, University Medical Centre Groningen, University of Groningen, 9713 GZ Groningen, The Netherlands.
Department of Pathology and Medical Biology, University Medical Centre Groningen, University of Groningen, 9713 GZ Groningen, The Netherlands.
Antioxidants (Basel). 2024 Oct 11;13(10):1224. doi: 10.3390/antiox13101224.
Systemic lupus erythematosus (SLE) is a complex autoimmune disease in which kidney involvement, so-called lupus nephritis (LN), is common and one of the most severe manifestations. Oxidative stress (OS) may play a role in the pathogenesis of LN through the exacerbation of inflammation and immune cell dysfunction/dysregulation. Nuclear factor erythroid 2-related factor 2 (Nrf2), also known as nuclear factor erythroid-derived 2-like 2, is a transcription factor that in humans is encoded by the NFE2L2 gene and is regarded as a central regulator of the antioxidative response. Nrf2-activating compounds have been shown to alleviate oxidative stress in cells and tissues of lupus-prone mice. Although the precise mechanisms of Nrf2 activation on the immune system in SLE remain to be elucidated, Nrf2-activating compounds are considered novel therapeutical options to suppress OS and thereby might alleviate disease activity in SLE, especially in LN. This review therefore summarizes the role of the Nrf2 signaling pathway in the pathogenesis of SLE with LN and describes compounds modulating this pathway as potential additional clinical interventions.
系统性红斑狼疮（SLE）是一种复杂的自身免疫性疾病，其中肾脏受累，即所谓的狼疮性肾炎（LN）很常见，也是最严重的表现之一。氧化应激（OS）可能通过加剧炎症和免疫细胞功能障碍/失调在LN的发病机制中起作用。核因子红细胞2相关因子2（Nrf2），也称为核因子红细胞衍生2样2，是一种转录因子，在人类中由NFE2L2基因编码，被视为抗氧化反应的核心调节因子。已证明Nrf2激活化合物可减轻易患狼疮小鼠细胞和组织中的氧化应激。尽管Nrf2激活对SLE免疫系统的确切机制仍有待阐明，但Nrf2激活化合物被认为是抑制OS的新型治疗选择，从而可能减轻SLE，尤其是LN的疾病活动。因此，本综述总结了Nrf2信号通路在LN型SLE发病机制中的作用，并将调节该通路的化合物描述为潜在的额外临床干预措施。
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