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Inhibition of iron ion accumulation alleviates polystyrene nanoplastics-induced pulmonary fibroblast proliferation and activation
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Researchers found that polystyrene nanoplastics (80 nm) caused lung cells to transform into scar-forming cells, a process that leads to pulmonary fibrosis, a serious and often irreversible lung disease. The key mechanism involved iron buildup in lung cells, which was triggered by interactions between immune cells and the nanoplastics. Importantly, blocking iron accumulation with an existing medication reversed the harmful effects, suggesting a potential treatment approach for nanoplastic-related lung damage.
Microplastics (MPs) and nanoplastics (NPs) are increasingly recognized as widespread environmental pollutants with significant ecological and human health implications, with particularly severe impacts on the respiratory system. This study aimed to explore the effects of polystyrene nanoplastics (PS-NPs, 80 nm) on pulmonary fibroblast proliferation and activation in NIH/3 T3 cells. Herein, we conducted a PS-NPs-induced fibroblast-to-myofibroblast transition (FMT) model and a pulmonary fibrosis mouse model. We found that PS-NPs effectively promoted fibroblast activation, proliferation, migration, and contraction. Fibroblast transcriptomics analyses revealed the enrichment of pathways involved in mineral absorption, mainly involved in iron ions, after PS-NPs treatment. Mechanistically, the elevated level of Fe in PS-NPs-stimulated NIH/3 T3 cells originated primarily from macrophages and epithelial cells, as validated by co-culture systems of fibroblasts with epithelial cells and fibroblasts with macrophages. Moreover, treatment with the iron chelator DFO and the mineral absorption pathway inhibitor Esomeprazole (a classic proton pump inhibitor, PPI) significantly reduced fibroblast activation. Consistent with the in vitro findings, in vivo results supported the occurrence of pulmonary fibrosis following PS-NPs exposure, accompanied by increased iron content in lung tissues. Collectively, these results revealed that PS-NPs could promote fibroblast activation and pulmonary fibrosis by augmenting intracellular iron content through enhancing epithelial-fibroblast and macrophage-fibroblast cross-talk. Therefore, our study also suggested that targeting intercellular crosstalk and iron homeostasis might be a promising therapeutic strategy for PS-NPs-induced pulmonary fibrosis.
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Ferritinophagy Mediated by Oxidative Stress-Driven Mitochondrial Damage Is Involved in the Polystyrene Nanoparticles-Induced Ferroptosis of Lung Injury
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Researchers found that inhaled polystyrene nanoplastics cause lung damage through a specific cell death process called ferroptosis, which involves iron buildup and oxidative stress in lung cells. The nanoplastics damaged mitochondria and triggered a chain reaction where the cell's iron storage was broken down, releasing harmful iron. Blocking this ferroptosis process with a drug called ferrostatin-1 reversed the lung damage in mice, pointing to a potential treatment approach.
Inhaled polystyrene microplastics impaired lung function through pulmonary flora/TLR4-mediated iron homeostasis imbalance
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Mice that inhaled polystyrene microplastics for 60 days developed lung scarring, reduced lung function, and weakened lung barriers. The microplastics increased harmful bacteria in the lungs, which triggered an iron-related cell death process called ferroptosis -- revealing a new mechanism by which breathing in microplastics could cause lasting lung damage.
Polystyrene nanoplastics lead to ferroptosis in the lungs
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Researchers found that polystyrene nanoplastics trigger ferroptosis — a type of iron-driven cell death — in the cells lining the lungs by activating a stress signaling pathway (HIF-1α/HO-1), ultimately causing lung tissue injury. This adds to growing evidence that inhaled nanoplastics can directly damage respiratory tissue through oxidative cell death mechanisms.
Polystyrene nanoplastics-induced lung epithelial cells ferroptosis promotes pulmonary fibrosis via YY1/FTL axis
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Researchers found that polystyrene nanoplastics induced ferroptosis—an iron-dependent form of cell death—in lung bronchial epithelial cells and promoted pulmonary fibrosis in mice via the YY1/FTL signaling axis. The study identified ferroptosis as a novel mechanism underlying nanoplastic-induced lung injury and fibrosis, with potential therapeutic relevance for targeting this pathway.
Polystyrene microplastics induce pulmonary fibrosis by promoting alveolar epithelial cell ferroptosis through cGAS/STING signaling
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Researchers found that mice exposed to polystyrene microplastics through their noses developed lung scarring (fibrosis) because the plastic particles triggered a form of cell death called ferroptosis, involving iron buildup and cell damage in lung tissue. Blocking the specific signaling pathway responsible (cGAS/STING) reduced the lung damage, pointing to a potential treatment approach if microplastic-related lung disease becomes a clinical concern.
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