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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.

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.