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61,005 resultsShowing papers similar to 5-methoxyindole-3-carboxaldehyde attenuates alveolar type II epithelial cell senescence induced by exposure to polystyrene microplastics in pulmonary fibrosis via PI3K/AKT/mTOR signaling pathway
ClearMicroplastics exposure causes the senescence of human lung epithelial cells and mouse lungs by inducing ROS signaling
Researchers found that four common types of microplastics all caused premature aging (senescence) in human lung cells by increasing harmful reactive oxygen species, and that an antioxidant treatment could partially reverse this effect. When PVC microplastics were introduced into mouse lungs, the animals showed reduced physical function, increased body-wide inflammation, and accumulation of aged cells, suggesting that inhaling microplastics could accelerate lung aging.
Tracing the cellular consequences of polyethylene microplastics: senescence and apoptosis in A549 and Raw 264.7 macrophage cells
Researchers exposed human lung epithelial cells (A549) and macrophages (Raw 264.7) to sub-500 nm polyethylene microplastics and found dose-dependent induction of cellular senescence and apoptosis. The results suggest that PE microplastic inhalation could contribute to premature lung cell aging and airway inflammation.
Microbial colonization of microplastics in wastewater accelerates the aging process associated with oxidative stress and the insulin/IGF1 signaling pathway
Researchers found that microbial colonization of polystyrene microplastics in wastewater accelerates their aging and increases toxicity in organisms, with biofilm-developed microplastics inducing oxidative stress and affecting lifespan through the insulin/IGF1 signaling pathway.
Inhaled polystyrene microplastics impaired lung function through pulmonary flora/TLR4-mediated iron homeostasis imbalance
Mice that inhaled polystyrene microplastics for 60 days developed lung scarring, reduced lung function, and weakened lung barriers. The microplastics increased harmful bacteria in the lungs, which triggered an iron-related cell death process called ferroptosis -- revealing a new mechanism by which breathing in microplastics could cause lasting lung damage.
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.
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.
Airborne polystyrene microplastics and nanoplastics induce nasal and lung microbial dysbiosis in mice
Researchers found that airborne polystyrene microplastics and nanoplastics can induce microbial dysbiosis in the nasal passages and lungs of mice. The study showed that both micro- and nanoplastics altered airway microbiota composition, with microplastics having a stronger influence on lung bacterial communities, suggesting that inhaled plastic particles may disrupt respiratory microbial balance.
Lung microbiota participated in fibrous microplastics (MPs) aggravating OVA-induced asthma disease in mice
In a mouse study, inhaling fiber-shaped microplastics significantly worsened asthma symptoms, including airway inflammation, mucus buildup, and lung tissue scarring. The microplastic fibers also disrupted the balance of bacteria living in the lungs and activated inflammatory pathways. Since fibrous microplastics are the most common airborne shape and have been found in human lungs, this research suggests they could worsen respiratory conditions like asthma in people.
Breathing plastics: Influence of airborne microplastics on the respiratory microbiome and health of human lungs (Review)
Researchers reviewed evidence showing that inhaled airborne microplastics can physically interact with the microbial community living in human lungs, disrupting its balance and triggering inflammation linked to conditions like asthma and fibrosis. Because microplastic particles have been found in lung tissue and fluid samples, inhalation is now recognized as a significant exposure route with measurable consequences for respiratory health.
Polystyrene Accelerates Aging Related-Gut Microbiome Dysbiosis and -Metabolites in Old-Aged Mouse
This mouse study investigated whether polystyrene microplastic exposure accelerates aging-related gut microbiome dysbiosis, using 16S rDNA sequencing and metabolomics. Polystyrene exposure disrupted the gut microbiota composition and altered fecal metabolite profiles in ways consistent with accelerated aging phenotypes.
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.
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.
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.
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.
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.
Microplastic-Induced Macrophage Dysfunction Drives Lung Tumor Progression through Glutathione Imbalance
Researchers found that microplastics trigger a cascade of immune dysfunction in macrophages through toll-like receptor signaling, leading to disrupted glutathione metabolism and macrophage cell death via ferroptosis. In tumor-bearing mice, orally ingested microplastics accumulated in the lungs and remodeled the immune microenvironment over time, with increased infiltration of inflammatory macrophages and impaired lymphocyte function accompanying greater tumor burden.
Polystyrene microplastics facilitate renal fibrosis through accelerating tubular epithelial cell senescence
Mice exposed to polystyrene microplastics at doses relevant to human exposure developed kidney inflammation and scarring (fibrosis) within 28 days. The microplastics caused kidney tube cells to age prematurely, triggering a chain reaction that activated scar-forming cells through a specific signaling pathway. This study provides evidence that microplastic exposure could contribute to chronic kidney damage in people.
Effects of secondary microplastic on the respiratory system of BALB/c mice
Researchers exposed BALB/c mice to secondary microplastics derived from environmentally weathered plastic and assessed respiratory system effects. Secondary MPs caused greater pulmonary inflammation and oxidative stress than virgin particles, suggesting that real-world aged plastics carry higher respiratory toxicity risks than pristine particles used in most laboratory studies.
Polyethylene terephthalate microplastics promote pulmonary fibrosis via AKT1, PIK3CD, and PIM1: A network toxicology and multi-omics analysis
Using computational toxicology and multi-omics analysis, researchers identified three key proteins (AKT1, PIK3CD, and PIM1) through which PET microplastics may promote pulmonary fibrosis, a serious scarring disease of the lungs. The microplastics appear to affect metabolic and inflammatory pathways in specific lung and immune cells. This study provides molecular evidence for how inhaled plastic particles from everyday items could contribute to chronic lung disease.
Polystyrene microplastics induce autophagy and apoptosis in birds lungs via PTEN/PI3K/AKT/mTOR
Researchers exposed broiler chickens to different concentrations of polystyrene microplastics and examined the effects on their lungs. They found that microplastics triggered cell death and autophagy in lung tissue through a specific signaling pathway involving PTEN, PI3K, AKT, and mTOR. The study provides evidence that inhaled microplastics can cause significant lung damage in birds, which serve as useful bioindicators for monitoring environmental pollution.
Detrimental effects of microplastic exposure on normal and asthmatic pulmonary physiology
Researchers exposed both healthy and asthmatic mice to airborne microplastics and found significant lung inflammation, immune activation, and increased mucus production in both groups. Microplastic particles were taken up by immune cells called macrophages, and gene analysis revealed changes in immune response, cellular stress, and cell death pathways. The study suggests that inhaling microplastics may worsen respiratory health in both normal and vulnerable populations.
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.
Polyethylene Micro/Nanoplastics Exposure Induces Epithelial–Mesenchymal Transition in Human Bronchial and Alveolar Epithelial Cells
When human lung cells were exposed to polyethylene micro- and nanoplastics (the most common type of plastic pollution), the cells underwent a transformation called epithelial-mesenchymal transition, where they changed shape, reorganized their internal structure, and gained increased ability to migrate. This cellular change is a known early step in both lung fibrosis and cancer development, suggesting that inhaling polyethylene plastics could contribute to serious lung diseases.
Pulmonary Flora‐Derived Lipopolysaccharide Mediates Lung‐Brain Axis through Activating Microglia Involved in Polystyrene Microplastic‐Induced Cognitive Dysfunction
In a mouse study, inhaling polystyrene microplastics impaired learning and memory -- even though the plastics never reached the brain directly. Instead, the microplastics changed the bacterial community in the lungs, which produced inflammatory signals that traveled to the brain and triggered damage, revealing a lung-to-brain pathway for microplastic harm.