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Mechanismof S‑Palmitoylationin Polystyrene Nanoplastics-Induced Macrophage Cuproptosis Contributingto Emphysema through Alveolar Epithelial Cell Pyroptosis
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Researchers identified S-palmitoylation—a lipid modification process—as a key mechanism by which inhaled polystyrene nanoplastics trigger macrophage ferroptosis (iron-dependent cell death) in the lungs, providing a molecular explanation for how respiratory nanoplastic exposure damages immune cells.
More than microplastics, nanoplastics may pose a greater toxic effect on humans due to their unique physicochemical properties. Currently, research on lung diseases caused by respiratory exposure to nanoplastics is scarce, with epigenetic mechanisms warranting further investigation. In the present study, we exposed rats to polystyrene nanoplastics (PS-NPs) via an oral-nasal exposure system and found that PS-NPs exposure resulted in emphysema. Mechanistically, PS-NPs entered macrophages and competitively bound to sigma nonopioid intracellular receptor 1 (SIGMAR1), leading to an increase in free zDHHC palmitoyltransferase 14 (zDHHC14). This, in turn, caused elevated palmitoylation of solute carrier family 31 member 1 (SLC31A1) in macrophages, inhibiting its ubiquitination and degradation, thereby enhancing SLC31A1 expression. The increased expression of SLC31A1 promoted cuproptosis of macrophages and elevated tumor necrosis factor-α (TNF-α) secretion, which activated the NLR family pyrin domain containing 3/matrix metallopeptidase 9 (NLRP3/MMP-9) pathway in alveolar epithelial cells (AECs). This process mediated pyroptosis and degradation of extracellular matrix (ECM), resulting in the destruction of alveolar structure and development of emphysema. The findings demonstrate a previously unknown molecular mechanism by which PS-NPs induce emphysema. The findings have implications for the prevention and treatment of respiratory system damage caused by nanoparticles.
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Mechanism of S-Palmitoylation in Polystyrene Nanoplastics-Induced Macrophage Cuproptosis Contributing to Emphysema through Alveolar Epithelial Cell Pyroptosis
AI summary Read the abstract
Researchers found that breathing in polystyrene nanoplastics caused emphysema (a type of lung disease) in rats by triggering a chain reaction: the nanoplastics entered immune cells in the lungs, caused copper-related cell death in those immune cells, which then released inflammatory signals that destroyed the air sacs. This newly discovered mechanism shows how inhaled nanoplastics could contribute to serious, irreversible lung damage.
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.
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.
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