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61,005 resultsShowing papers similar to Polystyrene nanoplastics induce pulmonary oxidative stress and programmed cell death through the cGAS-STING-NLRP3 pathway
ClearNasal 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.
Polystyrene nanoplastics mediate oxidative stress, senescence, and apoptosis in a human alveolar epithelial cell line
A cell study found that polystyrene nanoplastics cause dose-dependent damage to human lung cells, triggering oxidative stress, premature cell aging, and cell death. These findings suggest that breathing in nanoplastics could harm lung tissue over time and potentially contribute to cancer risk from air pollution.
Polystyrene nanoplastics-induced lung apoptosis and ferroptosis via ROS-dependent endoplasmic reticulum stress
This study found that polystyrene nanoplastics cause lung cell death through two pathways: apoptosis (programmed cell death) and ferroptosis (iron-dependent cell death), both triggered by oxidative stress in the cell's endoplasmic reticulum. The damage was observed both in human lung cells in the lab and in mice exposed to the nanoplastics. Importantly, the antioxidant NAC (N-acetylcysteine) reduced both types of cell death, suggesting it could help protect lungs from nanoplastic damage.
Polystyrene nanoplastics lead to ferroptosis in the lungs
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.
Intratracheal administration of polystyrene microplastics induces pulmonary fibrosis by activating oxidative stress and Wnt/β-catenin signaling pathway in mice
Researchers administered polystyrene microplastics directly into the lungs of mice and found that the particles induced pulmonary fibrosis by triggering oxidative stress and activating the Wnt signaling pathway. The microplastics caused damage to the lung lining cells and promoted the buildup of scar tissue in lung tissue. The study provides evidence that inhaled microplastics may contribute to serious respiratory conditions by driving fibrotic changes in the lungs.
Acute exposure to polystyrene nanoplastics induces unfolded protein response and global protein ubiquitination in lungs of mice
Mice exposed to polystyrene nanoplastics through their airways showed signs of cellular stress in lung tissue, including activation of the unfolded protein response (a defense mechanism cells use when proteins are damaged) and increased protein breakdown. The effects were dose-dependent, with higher nanoplastic doses causing more cellular distress. This research reveals a specific mechanism by which inhaled nanoplastics could damage lung cells, raising concerns about airborne microplastic exposure.
Investigation of pulmonary toxicity evaluation on mice exposed to polystyrene nanoplastics: The potential protective role of the antioxidant N-acetylcysteine
Researchers investigated lung damage in mice exposed to inhaled polystyrene nanoplastics and tested whether the antioxidant N-acetylcysteine could offer protection. They found that nanoplastics caused significant lung inflammation, tissue damage, and oxidative stress, but N-acetylcysteine treatment helped reduce these harmful effects. The study suggests that oxidative stress is a key mechanism behind nanoplastic-induced lung injury and points to potential protective strategies.
Gasdermin D-dependent macrophage pyroptosis mediates polystyrene microplastics-induced pulmonary fibrosis
Researchers demonstrated that chronic intranasal exposure to polystyrene microplastics in mice triggered a specific form of inflammatory cell death called pyroptosis in lung macrophages, leading to pulmonary fibrosis. The study identified the Gasdermin D protein as a key mediator of this process, suggesting a potential mechanistic pathway through which microplastic inhalation could contribute to lung tissue scarring.
In vitro evaluation of nanoplastics using human lung epithelial cells, microarray analysis and co-culture model
Researchers tested polystyrene nanoplastics on two types of human lung cells and found that the particles caused cell damage, oxidative stress, and inflammation-related gene changes at relatively low concentrations. Using a co-culture model that mimics the lung's layered structure, they showed that nanoplastics can trigger immune responses even in cells not directly exposed. The study suggests that inhaled nanoplastics may pose respiratory health risks through both direct toxicity and inflammatory signaling.
Polystyrene Nanoplastics Induce Lung Injury via Activating Oxidative Stress: Molecular Insights from Bioinformatics Analysis
Researchers found that polystyrene nanoplastics induce lung cell injury through oxidative stress pathways, identifying key transcription factors and the molecule TNFRSF12A as crucial mediators of nanoplastic-triggered redox imbalance and respiratory damage.
Sterile inflammation induced by respirable micro and nano polystyrene particles in the pathogenesis of pulmonary diseases
Researchers exposed human lung and immune cells to polystyrene micro and nanoparticles and found they triggered a type of inflammation that does not require infection, called sterile inflammation. Aged (oxidized) particles and those that interacted with immune cells were especially potent at activating inflammatory pathways including the NLRP3 inflammasome. This suggests that breathing in airborne microplastics could cause chronic lung inflammation over time.
Polystyrene nanoplastics induced lung injury in mice: Insights into lung metabolic disorders
Researchers exposed mice to polystyrene nanoplastics through the airway and found that the particles caused lung inflammation and tissue damage. Using metabolomics analysis, they discovered that the nanoplastics disrupted multiple metabolic pathways in lung tissue, with surface-modified particles causing more severe effects. The study provides evidence that inhaled nanoplastics can alter lung metabolism in ways that may contribute to respiratory health problems.
Exposure to polystyrene nanoplastics induces abnormal activation of innate immunity via the cGAS-STING pathway
Polystyrene nanoplastics triggered an abnormal immune response in mouse cells by activating a specific signaling pathway called cGAS-STING, which normally defends against viruses and damaged DNA. This activation led to inflammation through the NF-kB pathway, and when researchers silenced the STING gene, the inflammatory response was significantly reduced. The study reveals a new mechanism by which nanoplastics could cause chronic inflammation in the body.
Mechanism of S-Palmitoylation in Polystyrene Nanoplastics-Induced Macrophage Cuproptosis Contributing to Emphysema through Alveolar Epithelial Cell Pyroptosis
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.
Dynamic non-coding RNA biomarker reveals lung injury and repair induced by polystyrene nanoplastics
Researchers found that mice and lung organoids (lab-grown mini-organs) repeatedly exposed to polystyrene nanoplastics suffered lung tissue damage, impaired repair processes, and changes in non-coding RNA molecules that could serve as early warning biomarkers for nanoplastic-induced lung injury.
Ferritinophagy Mediated by Oxidative Stress-Driven Mitochondrial Damage Is Involved in the Polystyrene Nanoparticles-Induced Ferroptosis of Lung Injury
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.
Internalization and toxicity: A preliminary study of effects of nanoplastic particles on human lung epithelial cell
Researchers studied the effects of polystyrene nanoplastic particles on human lung cells and found that the particles were internalized by the cells and caused dose-dependent toxicity. The nanoplastics triggered oxidative stress, inflammation, and disrupted normal cell function. The findings suggest that inhaling airborne nanoplastics may pose risks to respiratory health.
Exposure to polystyrene microplastics triggers lung injury via targeting toll-like receptor 2 and activation of the NF-κB signal in mice
This mouse study found that inhaling polystyrene microplastics caused serious lung damage, including inflammation, cell death, and scar tissue buildup. Smaller microplastics (1-5 micrometers) caused more harm than larger ones, and the damage worsened with longer exposure. The study identified a specific immune pathway (TLR2/NF-kB) through which inhaled microplastics trigger lung injury, raising concerns about the respiratory effects of airborne microplastics on humans.
Unmodified Polystyrene Nanoparticles Induce Inflammatory and Oxidative Stress Responses in Human Lung Epithelial Cells
Exposure of human lung epithelial cells to unmodified polystyrene nanoparticles (60 nm) at concentrations as low as 50 µg/mL reduced cell viability by about 50% and triggered expression of inflammatory genes including IL-6 and CXCL10. These results suggest that nanoplastic particles reaching the respiratory tract could provoke lung inflammation, raising concerns about the health consequences of inhaling airborne nanoplastics.
Characterisation of changes in global genes expression in the lung of ICR mice in response to the inflammation and fibrosis induced by polystyrene nanoplastics inhalation
Researchers exposed mice to inhaled polystyrene nanoplastics for two weeks and used microarray analysis to identify 115 differentially expressed lung genes, with inflammation and fibrosis pathways significantly upregulated — findings that propose specific gene biomarkers for monitoring nanoplastic-induced pulmonary damage.