Ling Hong, Xiao Hong, Luo Ting, Lin Huicai, Deng Jiang
Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi 563006, China.
Key Laboratory of Basic Pharmacology of Guizhou Province, Zunyi Medical University, Zunyi 563006, China.
Biomedicines. 2023 Jan 9;11(1):163. doi: 10.3390/biomedicines11010163.
Idiopathic pulmonary fibrosis is a chronic interstitial lung disease whose pathogenesis involves a complex interaction of cell types and signaling pathways. Lung epithelial cells responding to repeated injury experience persistent inflammation and sustained epithelial-mesenchymal transition (EMT). The persistence of EMT-induced signals generates extracellular matrix accumulation, thereby causing fibrosis. Ferroptosis is a newly characterized iron-dependent non-apoptotic regulated cell death. Increased iron accumulation can increase iron-induced oxidant damage in alveolar epithelial cells. Studies have demonstrated that iron steady states and oxidation steady states play an important role in the iron death regulation of EMT. This review summarizes the role of ferroptosis in regulating EMT in pulmonary fibrosis, aiming to provide a new idea for the prevention and treatment of this disease.
特发性肺纤维化是一种慢性间质性肺疾病，其发病机制涉及多种细胞类型和信号通路的复杂相互作用。对反复损伤作出反应的肺上皮细胞会经历持续的炎症和持续的上皮-间质转化（EMT）。EMT诱导信号的持续存在会导致细胞外基质积累，从而引起纤维化。铁死亡是一种新发现的铁依赖性非凋亡性调节性细胞死亡。铁积累增加会增加铁诱导的肺泡上皮细胞氧化损伤。研究表明，铁稳态和氧化稳态在EMT的铁死亡调节中起重要作用。本文综述了铁死亡在调节肺纤维化EMT中的作用，旨在为该疾病的防治提供新思路。
