Remarkable contribution of particulate matter-induced macrophage ferroptosis to the pathology of pulmonary fibrosis

Guangzhe Zheng, S. Bi, Jiayu Ren, Sijin Liu, Bin Shi
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引用次数: 1

Abstract

Occupational exposure to particulate matter (PM) induced pulmonary fibrosis has aroused broad public concern. Pulmonary interstitial fibrosis is a central pathologic process of pneumoconiosis. Meanwhile, ferroptosis is a newly defined iron-dependent programmed cell death (PCD) that features increased intracellular labile iron and lethal accumulation of lipid peroxidation. Ferroptosis has been found to involve particulate-induced cytotoxicity. Recent studies have suggested that ferroptosis is closely associated with the occurrence and progression of pulmonary fibrosis. Here, we present a mini review to summarize the main mechanisms responsible for PM-induced pulmonary fibrosis via inducing macrophage ferroptosis to provide new insights into basic and clinical research of pulmonary fibrosis.
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颗粒物质诱导的巨噬细胞铁下垂对肺纤维化病理的显著贡献
职业性接触颗粒物(PM)诱发的肺纤维化引起了广泛关注。肺间质纤维化是尘肺病的中心病理过程。同时,铁死亡是一种新定义的铁依赖性程序性细胞死亡(PCD),其特征是细胞内不稳定铁增加和脂质过氧化的致命积累。已发现铁下垂与颗粒诱导的细胞毒性有关。近年来的研究表明,铁下垂与肺纤维化的发生和发展密切相关。在此,我们就pm通过诱导巨噬细胞铁上沉导致肺纤维化的主要机制进行综述,以期为肺纤维化的基础和临床研究提供新的见解。
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