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61,005 resultsShowing papers similar to Mechanisms of exacerbation of Th2-mediated eosinophilic allergic asthma induced by plastic pollution derivatives (PPD): A molecular toxicological study involving lung cell ferroptosis and metabolomics
ClearInhaled 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.
Mechanisms underlying Th2-dominant pneumonia caused by plastic pollution derivatives (PPD): A molecular toxicology investigation that encompasses gut microbiomics and lung metabolomics
In a mouse study, exposure to dibutyl phthalate (a plastic additive) and polystyrene microplastics for five weeks caused pneumonia-like lung damage, increased oxidative stress, and triggered inflammation. The researchers found that these plastic pollution byproducts caused a specific type of immune response that leads to eosinophilic inflammation in the airways, connected through the gut-lung axis. The findings suggest that everyday exposure to plastic-derived chemicals and particles could contribute to respiratory disease.
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.
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.
Microplastic exposure aggravates pneumococcus-induced inflammation in macrophages by activating ferroptosis
Researchers investigated how microplastic exposure affects the immune response of macrophages to pneumococcal (Streptococcus pneumoniae) infection. They found that microplastics impaired macrophage phagocytosis, inhibited bacterial clearance, and amplified inflammation by activating ferroptosis and promoting M1 macrophage polarization through PI3K/Akt and MAPK/ERK signaling pathways. The study suggests that microplastic exposure may worsen bacterial lung infections by compromising immune cell function.
Microplastics exacerbate ferroptosis via mitochondrial reactive oxygen species-mediated autophagy in chronic obstructive pulmonary disease
Researchers found that microplastics worsen chronic obstructive pulmonary disease (COPD) by triggering a chain reaction in lung cells: the plastics damage mitochondria (the cell's energy centers), which produces harmful molecules that activate a self-destructive process called autophagy-dependent ferroptosis. Lung tissue from COPD patients contained significantly higher concentrations of polystyrene microplastics than healthy controls. When scientists blocked this destructive pathway in mice, it reduced the excessive inflammation and prevented COPD flare-ups caused by microplastic exposure.
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.
Ferroptosis induced by environmental pollutants and its health implications
Researchers reviewed how environmental pollutants — including microplastics, PM2.5, and heavy metals — trigger ferroptosis, a form of programmed cell death driven by iron and fat oxidation, finding that targeting this cell death pathway could be a strategy to reduce organ damage caused by pollution exposure.
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.
Realistic Nanoplastics Induced Pulmonary Damage via the Crosstalk of Ferritinophagy and Mitochondrial Dysfunction
Researchers created realistic nanoplastics by mechanically breaking down bulk plastic rather than using lab-made particles, and found that inhaling these particles caused significant lung damage in mice through iron-related cell death and mitochondrial dysfunction. PVC nanoplastics were the most harmful of the four types tested, and all were more toxic than commonly used lab-standard polystyrene spheres, suggesting previous studies may have underestimated the lung health risks of airborne nanoplastics.
Cellular and molecular mechanisms of allergic asthma
Researchers reviewed the cellular and molecular mechanisms behind allergic asthma, finding that rising exposure to environmental pollutants — including microplastics — likely contributes to the disease's increasing prevalence, as pollutants disrupt airway barrier integrity and trigger immune responses that lead to chronic airway inflammation.
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.
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.
Ferroptosis participated in inhaled polystyrene nanoplastics-induced liver injury and fibrosis
Mice that inhaled polystyrene nanoplastics for up to 12 weeks developed liver injury and scarring (fibrosis), with damage worsening over time and at higher doses. The nanoplastics triggered a specific type of cell death called ferroptosis, which involves iron-dependent damage to cell membranes in the liver. This is one of the first studies to show that breathing in nanoplastics can cause serious liver damage, raising concerns about long-term health effects from airborne plastic pollution.
Polystyrene exacerbates cadmium‐induced mitochondrial damage to lung by blocking autophagy in mice
Researchers found that polystyrene microplastics exacerbated cadmium-induced mitochondrial damage in mouse lungs by blocking autophagy, revealing a synergistic toxicity mechanism when these two common environmental contaminants co-occur.
Presence of nanoplastics in sputum of patients with severe asthma: a novel environmental perspective
Researchers analyzed sputum from severe asthma patients and detected nanoplastics in samples for the first time, comparing concentrations and immune profiles across asthma phenotypes. Nanoplastic presence in sputum was associated with more severe disease and distinct immune dysregulation patterns, identifying environmental nanoplastic exposure as a potential modifier of asthma severity.
Impact of Microplastic Exposure on Airway Inflammation in an Acute Asthma Murine Model
Mouse experiments found that microplastic exposure worsened inflammatory responses in healthy lungs but did not further aggravate airway inflammation in mice with pre-existing asthma, suggesting the lung's response to microplastics depends on baseline immune state.
Co-exposure to polyethylene microplastics and house dust mites aggravates airway epithelial barrier dysfunction and airway inflammation via CXCL1 signaling pathway in a mouse model
In a mouse model of asthma, co-exposure to inhaled polyethylene microplastics and house dust mite allergens caused worse airway inflammation than either pollutant alone. The microplastics damaged the airway lining and amplified allergic reactions through a specific inflammatory signaling pathway called CXCL1. This finding suggests that breathing in airborne microplastics could make allergies and asthma worse by helping allergens penetrate deeper into the lungs.
Understanding the mechanistic roles of microplastics combined with heavy metals in regulating ferroptosis: Adding new paradigms regarding the links with diseases
This review explores the emerging connection between microplastics combined with heavy metals and a type of cell death called ferroptosis, which involves iron-dependent damage to cell membranes. Researchers found that both microplastics and heavy metals can independently trigger ferroptosis, and their combined presence may amplify this effect in organs like the liver, kidneys, and brain. The study suggests that understanding this cell death pathway could provide new insights into how environmental pollutant mixtures contribute to disease.
Co-exposure to polystyrene microplastics and di-(2-ethylhexyl) phthalate aggravates allergic asthma through the TRPA1-p38 MAPK pathway
This mouse study found that polystyrene microplastics combined with DEHP, a common plastic additive, worsened allergic asthma symptoms more than either pollutant alone. The combination activated an inflammatory pathway called TRPA1-p38 MAPK in lung tissue, increasing airway inflammation and mucus production. The findings suggest that real-world exposure to microplastics carrying chemical additives could aggravate respiratory conditions like asthma.
Microplastic exposure induces preeclampsia-like symptoms via HIF-1α/TFRC-mediated ferroptosis in placental trophoblast cells
Researchers exposed pregnant rats to polystyrene microplastics and found that the particles induced symptoms resembling preeclampsia, including elevated blood pressure and increased protein in urine. The microplastics triggered a type of cell death called ferroptosis in placental cells by activating a specific signaling pathway that led to iron overload and oxidative damage. The study identifies microplastic-induced placental cell death as a potential mechanism linking environmental plastic exposure to pregnancy complications.
Polystyrene nanoplastics-induced lung epithelial cells ferroptosis promotes pulmonary fibrosis via YY1/FTL axis
Researchers found that polystyrene nanoplastics induced ferroptosis—an iron-dependent form of cell death—in lung bronchial epithelial cells and promoted pulmonary fibrosis in mice via the YY1/FTL signaling axis. The study identified ferroptosis as a novel mechanism underlying nanoplastic-induced lung injury and fibrosis, with potential therapeutic relevance for targeting this pathway.
Implication of ferroptosis in hepatic toxicity upon single or combined exposure to polystyrene microplastics and cadmium
This study found that polystyrene microplastics combined with cadmium caused more severe liver damage in mice than either pollutant alone. The microplastics absorbed cadmium on their surface, increasing the amount of the toxic metal delivered to liver cells, and triggered a type of cell death called ferroptosis. This is concerning because microplastics in the environment commonly carry heavy metals, meaning the combined exposure people face may be more harmful than we thought.
Co-exposure of polystyrene microplastics and iron aggravates cognitive decline in aging mice via ferroptosis induction
Researchers studied the combined effects of microplastic and iron exposure on cognitive function in aging mice. They found that polystyrene microplastics accumulated in the brain's cortex and hippocampus, and when combined with iron, significantly worsened cognitive decline through a cell death process called ferroptosis. The study suggests that co-exposure to microplastics and metals may pose heightened risks to brain health in aging populations.