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61,005 resultsShowing papers similar to A study on the roles of long non-coding RNA and circular RNA in the pulmonary injuries induced by polystyrene microplastics
ClearDynamic 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.
Mechanism of circRNA_SMG6 mediating lung macrophage ECM degradation via miR-570-3p in microplastics-induced emphysema
In a rat study, inhaling polystyrene microplastics for 90 days caused lung damage resembling emphysema, including inflammation, thickened tissue walls, and enlarged air sacs. The microplastics triggered the breakdown of the structural support network in the lungs through a specific molecular pathway involving circular RNA. This research provides a mechanism by which breathing in microplastic particles could contribute to chronic lung disease in humans.
The regulation of circRNA_kif26b on alveolar epithelial cell senescence via miR-346-3p is involved in microplastics-induced lung injuries
Researchers found that inhaled polystyrene microplastics caused lung damage in rats by accelerating the aging of cells lining the air sacs, through a specific molecular pathway involving circular RNA. The microplastics triggered inflammation, fibrosis, and premature cell aging in lung tissue over a 35-day exposure period. The study reveals a new mechanism by which inhaled microplastics may contribute 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.
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.
Functional roles of circular RNAs in lung injury
This review examines the functional roles of circular RNAs in various forms of lung injury, including their involvement in disease progression. The study suggests that understanding circRNA mechanisms could lead to new insights into respiratory damage pathways, though the connection to environmental exposures requires further investigation.
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 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.
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.
Deleterious effects of microplastics and nanoplastics on rodent lungs: a systematic review
This systematic review summarizes research on how inhaled micro- and nanoplastics affect the lungs in animal studies. The findings show these particles can cause lung inflammation, tissue damage, and immune responses, suggesting that breathing in airborne microplastics may pose real risks to respiratory health.
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.
Potential health risks of the interaction of microplastics and lung surfactant
Researchers investigated how polystyrene microplastics interact with lung surfactant extracted from porcine lungs. The study found that microplastics altered the surface tension and membrane structure of lung surfactant, preferentially adsorbed phospholipid components, and accelerated the production of reactive oxygen species, suggesting potential risks to respiratory health from inhaled microplastics.
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.
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.
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.
Lung hazards of microplastics and their toxicological mechanisms
This review summarizes eight key mechanisms by which microplastics cause lung injury, including oxidative stress, inflammation, DNA damage, and disruption of the immune response. Researchers explain how the small size and large surface area of microplastics allow them to evade respiratory clearance and deposit deep in lung tissue. The study provides a comprehensive framework for understanding how inhaled microplastics may contribute to respiratory health problems.
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.
Inflammatory Effects of Microplastics and Nanoplastics on Nasal Airway Epithelial Cells
Researchers found that polystyrene micro- and nanoplastics cause inflammatory cytokine responses in nasal epithelial cells even over short exposure periods. The study also observed ciliary blunting and transcriptional evidence of significant inflammation and stress responses, suggesting that the nasal airway is vulnerable to plastic particle exposure.
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.
Lung retention, distribution and persistence of polymer particles in rats exposed via inhalation
Researchers studied the fate of inhaled polymer particles in rats by exposing them to polystyrene and polyamide aerosols for 28 days. The study found that both types of particles accumulated in the lungs and migrated to lung-draining lymph nodes, but were not detected in the liver, spleen, or kidneys. The particles persisted in lung tissue for weeks after exposure ended, highlighting potential concerns about long-term retention of inhaled microplastics.
Intratracheal 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.
Lung retention, distribution and persistence of polymer particles in rats exposed via inhalation
Researchers studied the fate of inhaled polymer particles in rats by exposing them to polystyrene and polyamide aerosols for 28 days. The study found that both types of particles accumulated in the lungs and migrated to lung-draining lymph nodes, but were not detected in the liver, spleen, or kidneys. The particles persisted in lung tissue for weeks after exposure ended, raising questions about the long-term bioavailability and fate of inhaled microplastics.
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.
Inhalation of Microplastics Induces Inflammatory Injuries in Multiple Murine Organs via the Toll-like Receptor Pathway
After mice inhaled polystyrene microplastics, the particles spread to the brain, liver, kidneys, spleen, and other organs within days, triggering widespread inflammation through a specific immune signaling pathway called TLR/NF-kB. These findings suggest that breathing in microplastics could cause inflammatory damage across multiple organ systems in the body.