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61,005 resultsShowing papers similar to Dynamic non-coding RNA biomarker reveals lung injury and repair induced by polystyrene nanoplastics
ClearA study on the roles of long non-coding RNA and circular RNA in the pulmonary injuries induced by polystyrene microplastics
Researchers exposed rats to polystyrene microplastics through the airways and found evidence of lung tissue damage, including destroyed air sacs and inflammation. The study identified changes in the activity of long non-coding RNAs and circular RNAs, types of genetic regulators that may help explain how microplastics cause lung injury at the molecular level. These findings provide new insight into the biological mechanisms behind potential respiratory harm from inhaling microplastic particles.
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.
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.
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.
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.
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.
Repeated inhalation exposure to polystyrene nanoplastics induced sustained pulmonary injury and fibrosis in mice.
Scientists exposed mice to tiny plastic particles found in air pollution and discovered these particles caused serious lung damage and scarring that didn't heal even weeks after exposure stopped. The smallest plastic particles were the most harmful, spreading from the lungs to other organs like the heart and liver. This research suggests that breathing in nanoplastics from everyday sources like car tire wear and plastic waste could pose long-term risks to human lung health.
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 nanoplastics induce pulmonary oxidative stress and programmed cell death through the cGAS-STING-NLRP3 pathway
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.
Profiling of lincRNAs and differential regulatory mechanisms in response to nanoplastic toxicity at environmentally relevant concentrations in Caenorhabditis elegans
Researchers investigated how polystyrene nanoplastics at environmentally relevant concentrations affect long noncoding RNA expression in the model organism C. elegans. The study identified specific regulatory mechanisms involving lncRNAs in the toxic response to nanoplastic exposure, providing new insights into the molecular pathways through which nanoplastics may harm living organisms.
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.
Small Particles, Big Problems: Polystyrene nanoparticles induce DNA damage, oxidative stress, migration, and mitogenic pathways predominantly in non-malignant lung cells
Researchers exposed non-malignant and malignant lung cells as well as lung organoids to polystyrene micro- and nanoplastics at two sizes and measured DNA damage, oxidative stress, and cell migration. Non-malignant cells showed greater sensitivity than cancer cells, with the smaller 0.25 µm particles inducing more oxidative damage and migration at lower concentrations.
Pulmonary hazards of nanoplastic particles: a study using polystyrene in in vitro models of the alveolar and bronchial epithelium
Lab tests on human lung cell models found that polystyrene nanoplastics did not cause immediate cell death but did interfere with key lung functions like surfactant and mucus production and immune signaling. This means standard toxicity tests may underestimate the real danger of inhaling nanoplastics, and researchers need to look beyond simple cell survival to understand the true health effects on the lungs.
Comprehensive Analysis of lncRNA–mRNA Expression Profiles in Depression-like Responses of Mice Related to Polystyrene Nanoparticle Exposure
Researchers found that polystyrene nanoparticle exposure induced depression-like behaviors in mice and identified altered long non-coding RNA and mRNA expression profiles in brain tissue, revealing molecular pathways through which nanoplastics may affect neurological function.
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.
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.
Microplastics and nanoplastics, emerging pollutants, increased the risk of pulmonary fibrosis in vivo and in vitro: A comparative evaluation of their potential toxicity effects with different polymers and size
Researchers compared the lung toxicity of microplastics and nanoplastics made from polystyrene, polyethylene, and polypropylene in mice and human lung cells. They found that all particle types induced signs of pulmonary fibrosis, inflammation, and tissue remodeling, with polystyrene nanoplastics causing the most severe effects. The study suggests that smaller nanoplastic particles and certain polymer types may pose greater risks to lung health.
Inhaled polystyrene nanoparticles may cause fibrotic lesions via immune dysregulation and energy metabolism disturbance
Mice received polystyrene nanoparticles via pharyngeal instillation for 90 days and were assessed for local lung and systemic toxicity. The nanoparticles accumulated in lungs and hearts, caused immune dysregulation, disrupted energy metabolism, and induced fibrotic lesions at higher doses, suggesting that chronic inhalation of nanoplastics may contribute to pulmonary fibrosis.
Polystyrene microplastic particles: In vitro pulmonary toxicity assessment
Researchers tested the effects of polystyrene microplastics on human lung cells in the laboratory and found that the particles triggered inflammation and oxidative stress. The microplastics also weakened the protective barrier function of lung tissue by depleting key structural proteins. The study suggests that inhaling microplastics may increase the risk of respiratory problems by damaging the lung's natural defenses.
Size-dependent toxicity of polystyrene microplastics in lung cells: An in vivo and in vitro study
Researchers investigated the size-dependent toxicity of polystyrene microplastics in lung cells using both mouse and cell culture models. The study found that smaller 1-micrometer particles accumulated more in lung tissue than larger particles and identified epithelial-mesenchymal transition as a key toxic mechanism, driven by ECM-MMP signaling cascades that contribute to lung injury.
Uptake of Breathable Nano- and Micro-Sized Polystyrene Particles: Comparison of Virgin and Oxidised nPS/mPS in Human Alveolar Cells
Researchers found that environmentally aged (oxidised) nano- and microplastics were rapidly taken up by human lung cells and caused significantly greater DNA damage, oxidative stress, and mitochondrial impairment compared to pristine particles, highlighting the heightened health risks of weathered airborne plastics.
Polystyrene nanoplastics affect transcriptomic and epigenomic signatures of human fibroblasts and derived induced pluripotent stem cells: Implications for human health
Researchers found that polystyrene nanoplastics altered transcriptomic and epigenomic signatures in human fibroblasts and derived induced pluripotent stem cells, demonstrating that plastic particle exposure can cause lasting molecular changes with potential implications for human health.
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.
Integrated transcriptomics and metabolomics reveal the mechanism of polystyrene nanoplastics toxicity to mice
Researchers used gene expression and metabolic profiling to understand how polystyrene nanoplastics harm mice at the molecular level, finding disrupted energy metabolism, fat processing, and amino acid pathways in the liver. These molecular changes suggest that nanoplastic exposure could contribute to metabolic disorders, with effects becoming more severe at higher doses.