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20 resultsShowing papers similar to Intratracheal administration of polystyrene microplastics induces pulmonary fibrosis by activating oxidative stress and Wnt/β-catenin signaling pathway in mice
ClearIntratracheal Administration of Polystyrene Micro(nano)plastics with a Mixed Particle Size Promote Pulmonary Fibrosis in Rats by Activating TGF-β1 Signaling and Destabilizing Mitochondrial Dynamics and Mitophagy in a Dose- and Time-Dependent Manner.
SD rats exposed to mixed polystyrene micro(nano)plastics via intratracheal administration at escalating doses over time developed pulmonary fibrosis and mitochondrial dysfunction, with severity linked to dose. The findings demonstrated a clear biological pathway connecting inhaled microplastic exposure to lung injury.
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.
Oropharyngeal Administration of Polystyrene Microplastics Induces Profibrotic and Oxidative Changes in Murine Lung Tissue
Researchers investigated the early lung effects of inhaled polystyrene microplastics in mice over a 21-day exposure period. While overall fibrosis scores did not reach statistical significance in this short timeframe, they observed significant macrophage infiltration, active particle uptake by immune cells, and upregulation of oxidative stress and fibrosis-related molecular markers. The findings suggest that microplastic inhalation triggers early immune and oxidative responses that may precede lung tissue remodeling.
A particle of concern: explored and proposed underlying mechanisms of microplastic-induced lung damage and pulmonary fibrosis
This paper explores how inhaled microplastics may cause lung damage and scarring (pulmonary fibrosis) through several biological pathways. The research identifies signaling pathways that could be targeted for future treatments to reduce microplastic-induced lung damage. This is relevant to human health because people regularly breathe in airborne microplastic particles.
Polystyrene microplastics cause cardiac fibrosis by activating Wnt/β-catenin signaling pathway and promoting cardiomyocyte apoptosis in rats
Researchers exposed rats to polystyrene microplastics at varying concentrations for 90 days and examined cardiovascular effects. The study found that microplastic exposure activated the Wnt/beta-catenin signaling pathway and promoted cardiomyocyte apoptosis, leading to cardiac fibrosis, suggesting that chronic microplastic exposure may pose risks to cardiovascular health.
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 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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
The Effect of Subchronic Polyethylene Microplastic Exposure on Pulmonary Fibrosis Through Pro-Inflammatory Cytokines TNF-α and IL-1β in Wistar Rats
This animal study found that breathing in polyethylene microplastics over several weeks led to lung scarring (pulmonary fibrosis) in rats by triggering inflammatory immune responses. The results suggest that chronic inhalation of airborne microplastics could contribute to serious lung damage in humans, since we breathe in thousands of plastic particles daily.
Chronic lung tissue deposition of inhaled polyethylene microplastics may lead to fibrotic lesions
In a mouse study, inhaled polyethylene microplastics accumulated in lung tissue over 90 days of repeated exposure, causing chronic inflammation, immune changes, and early signs of lung scarring (fibrosis). Even at the lowest doses, the microplastics triggered inflammatory cell buildup and thickening of lung walls. These findings suggest that long-term breathing of airborne microplastics could lead to permanent lung damage, which is concerning given rising levels of plastic particles in indoor and outdoor air.
Polypropylene microplastic exposure leads to lung inflammation through p38-mediated NF- κB pathway due to mitochondrial damage
Researchers found that instilling polypropylene microplastic particles into mouse lungs caused dose-dependent increases in inflammatory cell counts, reactive oxygen species, and pro-inflammatory cytokines, with lung tissue analysis revealing the particles triggered inflammation via mitochondrial damage activating the p38-mediated NF-kB signaling pathway.