Author:
Ling Hong,Xiao Hong,Luo Ting,Lin Huicai,Deng Jiang
Abstract
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.
Funder
National Natural Science Foundation of China
APC
Subject
General Biochemistry, Genetics and Molecular Biology,Medicine (miscellaneous)
Cited by
14 articles.
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