Wang Chunyan, Hua Shucheng, Song Lei
Department of General Practice, Key Laboratory of Organ Regeneration and Transplantation of the Ministry of Education, The First Hospital of Jilin University, Changchun, China.
Department of Respiratory Medicine, Center for Pathogen Biology and Infectious Diseases, The First Hospital of Jilin University, Changchun, China.
Front Physiol. 2023 Aug 17;14:1205771. doi: 10.3389/fphys.2023.1205771. eCollection 2023.
In recent years, the role of ferroptosis in pulmonary fibrosis has garnered increasing interest as a potential therapeutic target. Pulmonary fibrosis is a pathological process characterized by the accumulation of extracellular matrix in affected lung tissues, and currently, there are no effective therapies for preventing or reversing the fibrotic lesions. Ferroptosis is a form of programmed cell death that is regulated by a network of enzymes and signaling pathways. Dysregulation of ferroptosis has been implicated in several diseases, including pulmonary fibrosis. The accumulation of lipid peroxides in the course of ferroptosis causes damage to cell membranes and other cellular components, leading ultimately to cell death. Relevant targets for therapeutic intervention in ferroptosis include key enzymes, such as glutathione peroxidase 4, transcription factors like nuclear factor erythroid 2-related factor 2, and iron chelation. This review provides an overview of the emerging role of ferroptosis in pulmonary fibrosis and highlights potential therapeutic targets in this pathway. Further research is needed to develop safe and effective approaches targeting ferroptosis in treatment of pulmonary fibrosis.
近年来，铁死亡在肺纤维化中的作用作为一个潜在的治疗靶点已引起越来越多的关注。肺纤维化是一种病理过程，其特征是在受影响的肺组织中细胞外基质的积累，目前，尚无有效的疗法来预防或逆转纤维化病变。铁死亡是一种程序性细胞死亡形式，受一系列酶和信号通路网络的调节。铁死亡的失调与包括肺纤维化在内的多种疾病有关。铁死亡过程中脂质过氧化物的积累会导致细胞膜和其他细胞成分受损，最终导致细胞死亡。铁死亡治疗干预的相关靶点包括关键酶，如谷胱甘肽过氧化物酶4、转录因子如核因子红细胞2相关因子2以及铁螯合。本文综述概述了铁死亡在肺纤维化中新兴的作用，并强调了该途径中的潜在治疗靶点。需要进一步研究以开发针对铁死亡治疗肺纤维化的安全有效方法。
