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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.
Nanoplastics (NPs) have emerged as pervasive environmental pollutants, and polystyrene nanoplastics (PS-NPs) have been increasingly implicated in pulmonary toxicity and fibrosis. Here, we established both an in vitro BEAS-2B bronchial epithelial injury model and an in vivo mouse model by repeated oropharyngeal aspiration of PS-NPs. We observed pronounced pulmonary fibrosis and ferroptotic death of alveolar type II cells. Integrated transcriptomic and proteomic profiling highlighted enrichment of the ferroptosis pathway, and in vitro and in vivo experiments confirmed that PS-NPs suppress GPX4 while inducing FTL, thereby driving lipid peroxidation. Mechanistically, YY1 binds the FTL promoter to repress its expression, and YY1 knockdown alleviates ferroptosis and fibrosis. Our findings identify YY1/FTL-mediated ferroptosis as a key mechanism by which PS-NPs induce 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.
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 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.
Ferroptosis participated in inhaled polystyrene nanoplastics-induced liver injury and fibrosis
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Mice that inhaled polystyrene nanoplastics for up to 12 weeks developed liver injury and scarring (fibrosis), with damage worsening over time and at higher doses. The nanoplastics triggered a specific type of cell death called ferroptosis, which involves iron-dependent damage to cell membranes in the liver. This is one of the first studies to show that breathing in nanoplastics can cause serious liver damage, raising concerns about long-term health effects from airborne plastic pollution.
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.
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