We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Polystyrene nanoplastics induce pulmonary oxidative stress and programmed cell death through the cGAS-STING-NLRP3 pathway
Summary
Researchers exposed mice to polystyrene nanoplastics through nasal administration and studied the resulting lung damage over seven days. They found that the nanoplastics triggered oxidative stress, programmed cell death, and inflammatory responses in lung tissue through activation of the cGAS-STING-NLRP3 signaling pathway. The study provides evidence that inhaled nanoplastics can cause acute lung injury through specific molecular mechanisms involving both apoptosis and pyroptosis.
Polystyrene nanoplastics(PS-NPs) in the atmosphere can be inhaled because of their small size. They will be deposited deep in the alveoli. This poses a major threat to respiratory health. The molecular mechanism of acute lung injury caused by them has not yet been fully clarified. This study established an acute mouse nasal drip model. The dose is 50 and 100 mg/kg respectively, and it can be used continuously for seven days. We evaluated the lung tissue damage and the activation of the cGAS-STING-NLRP3 pathway. The measurements carried out include oxidative stress markers and key apoptosis and cell pyrotosis proteins. Molecular docking simulation was also carried out. The results show that PS-NPs exposure leads to oxidative damage and apoptosis. This work systematically proved that inhaled PS-NPs triggers acute lung injury through the cGAS-STING-NLRP3 pathway. This discovery promotes the understanding of the toxicity mechanism of nanoplastics. It also identified this axis as a key target for future risk assessment and targeted treatment.
Sign in to start a discussion.
More Papers Like This
Nasal instillation of polystyrene nanoplastics induce lung injury via mitochondrial DNA release and activation of the cyclic GMP-AMP synthase-stimulator of interferon genes-signaling cascade
Researchers showed that inhaled polystyrene nanoplastics trigger lung fibrosis and inflammation in mice by inducing mitochondrial DNA release into the cytoplasm, which activates the cGAS-STING innate immune signaling pathway — a discovery that identifies a specific molecular mechanism linking nanoplastic inhalation to pulmonary injury.
Polystyrene microplastics induce pulmonary fibrosis by promoting alveolar epithelial cell ferroptosis through cGAS/STING signaling
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.
Unveiling the Pulmonary Toxicity of Polystyrene Nanoplastics: A Hierarchical Oxidative Stress Mechanism Driving Acute–Subacute Lung Injury
Researchers investigated the pulmonary toxicity of polystyrene nanoplastics smaller than 100 nm in lung epithelial cells and macrophages, finding that exposure triggered a hierarchical oxidative stress mechanism that drove acute to subacute lung injury through lipid peroxidation and inflammation.
Metabolomics reveals that PS-NPs promote lung injury by regulating prostaglandin B1 through the cGAS-STING pathway
Researchers found that polystyrene nanoplastics activate the cGAS-STING innate immune pathway in human lung cells and macrophages at near-environmental concentrations, causing mitochondrial dysfunction and metabolic disruption — and that supplementing prostaglandin B1, a nanoplastic-depleted metabolite, partially reversed these effects.
Inhalation exposure to polystyrene nanoplastics induces chronic obstructive pulmonary disease-like lung injury in mice through multi-dimensional assessment
Mice that inhaled polystyrene nanoplastics developed lung damage resembling chronic obstructive pulmonary disease (COPD), including reduced breathing function, inflammation, and oxidative stress that worsened with longer exposure. The study found that nanoplastics caused this damage by disrupting mitochondria and triggering a type of cell death called ferroptosis, suggesting that breathing in airborne nanoplastics could increase the risk of serious lung disease.