Deng JiaLi, Li Na, Hao Liyuan, Li Shenghao, Aiyu Nie, Zhang Junli, Hu XiaoYu
School of Clinical Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China.
Department of Infectious Disease, Jiangsu Province Hospital of Traditional Chinese Medicine, Nanjing, Jiangsu, China.
PeerJ. 2024 Jul 30;12:e17692. doi: 10.7717/peerj.17692. eCollection 2024.
NRF2 is an important transcription factor that regulates redox homeostasis and exerts its anti-oxidative stress and anti-inflammatory response by binding to the ARE to activate and regulate the transcription of downstream protective protein genes, reducing the release of reactive oxygen species. Ferroptosis is a novel iron-dependent, lipid peroxidation-driven cell death mode, and recent studies have shown that ferroptosis is closely associated with acute lung injury/acute respiratory distress syndrome (ALI/ARDS). NRF2 is able to regulate ferroptosis through the regulation of the transcription of its target genes to ameliorate ALI/ARDS. Therefore, This article focuses on how NRF2 plays a role in ALI/ARDS by regulating ferroptosis. We further reviewed the literature and deeply analyzed the signaling pathways related to ferroptosis which were regulated by NRF2. Additionally, we sorted out the chemical molecules targeting NRF2 that are effective for ALI/ARDS. This review provides a relevant theoretical basis for further research on this theory and the prevention and treatment of ALI/ARDS. The intended audience is clinicians and researchers in the field of respiratory disease.
NRF2是一种重要的转录因子,可调节氧化还原稳态,并通过与抗氧化反应元件(ARE)结合来激活和调节下游保护性蛋白基因的转录,从而发挥其抗氧化应激和抗炎反应,减少活性氧的释放。铁死亡是一种新型的铁依赖性、脂质过氧化驱动的细胞死亡模式,最近的研究表明,铁死亡与急性肺损伤/急性呼吸窘迫综合征(ALI/ARDS)密切相关。NRF2能够通过调节其靶基因的转录来调控铁死亡,从而改善ALI/ARDS。因此,本文重点探讨NRF2如何通过调节铁死亡在ALI/ARDS中发挥作用。我们进一步查阅文献,深入分析了NRF2调控的与铁死亡相关的信号通路。此外,我们梳理了对ALI/ARDS有效的靶向NRF2的化学分子。本综述为该理论的进一步研究以及ALI/ARDS的防治提供了相关理论依据。目标受众是呼吸疾病领域的临床医生和研究人员。