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61,005 resultsShowing papers similar to Ferritinophagy Mediated by Oxidative Stress-Driven Mitochondrial Damage Is Involved in the Polystyrene Nanoparticles-Induced Ferroptosis of Lung Injury
ClearPolystyrene 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.
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.
Polystyrene nanoplastics-induced lung apoptosis and ferroptosis via ROS-dependent endoplasmic reticulum stress
This study found that polystyrene nanoplastics cause lung cell death through two pathways: apoptosis (programmed cell death) and ferroptosis (iron-dependent cell death), both triggered by oxidative stress in the cell's endoplasmic reticulum. The damage was observed both in human lung cells in the lab and in mice exposed to the nanoplastics. Importantly, the antioxidant NAC (N-acetylcysteine) reduced both types of cell death, suggesting it could help protect lungs from nanoplastic damage.
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.
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.
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.
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.
Exposure of polystyrene nanoplastics led to ferroptosis on cardiomyocytes
Researchers exposed rat heart cells to 100-nanometer polystyrene nanoparticles and found that the particles were taken up by the cells and triggered a form of iron-dependent cell death called ferroptosis. The nanoparticles caused a buildup of reactive oxygen species in mitochondria, iron accumulation, and damage to cell membranes. The study suggests that nanoplastic exposure may pose risks to heart health through this specific cell death pathway.
Inhibition of iron ion accumulation alleviates polystyrene nanoplastics-induced pulmonary fibroblast proliferation and activation
Researchers found that polystyrene nanoplastics (80 nm) caused lung cells to transform into scar-forming cells, a process that leads to pulmonary fibrosis, a serious and often irreversible lung disease. The key mechanism involved iron buildup in lung cells, which was triggered by interactions between immune cells and the nanoplastics. Importantly, blocking iron accumulation with an existing medication reversed the harmful effects, suggesting a potential treatment approach for nanoplastic-related lung damage.
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.
Ferroptosis involved in inhaled polystyrene microplastics leaded myocardial fibrosis through HIF-ROS-SLC7A11/GPX4 Pathway
Researchers found that inhaling polystyrene microplastics caused heart muscle scarring (fibrosis) in mice through a process called ferroptosis, a type of iron-dependent cell death. The microplastics triggered a chain reaction involving low oxygen signals and oxidative stress that depleted the heart cells' protective antioxidant systems. This study reveals a specific mechanism by which breathing in airborne microplastics could lead to lasting heart damage.
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.
Inhalation exposure to cationic nanoplastic induces ferroptosis in the lung by perturbing core circadian transcription factors Bmal1
Researchers showed that inhaled cationic (positively charged, amino-modified) polystyrene nanoplastics trigger a form of iron-dependent cell death called ferroptosis in mouse lungs by suppressing the circadian clock protein Bmal1 and its downstream antioxidant pathway, and that a natural Bmal1 activator partially protected against the damage.
Polystyrene nanoplastics disrupt iron homeostasis by promoting FPN1 ubiquitination in GC-2spd(ts) cells
Researchers showed that polystyrene nanoplastics induce ferroptosis — an iron-dependent form of cell death — in mouse sperm precursor cells by promoting the ubiquitin-tagged degradation of the iron-export protein ferroportin1, causing iron to accumulate inside cells, driving lipid peroxidation and mitochondrial damage.
Internalized polystyrene nanoplastics trigger testicular damage and promote ferroptosis via CISD1 downregulation in mouse spermatocyte
Researchers found that polystyrene nanoplastics cause testicular damage in mice through a cell death process called ferroptosis. The nanoplastics triggered the breakdown of iron-storage proteins and reduced levels of a protective mitochondrial protein called CISD1 in sperm cells. The study suggests that nanoplastic exposure may contribute to male reproductive harm by driving excess iron into mitochondria.
Polystyrene nanoplastic exposure actives ferroptosis by oxidative stress-induced lipid peroxidation in porcine oocytes during maturation
Researchers found that polystyrene nanoplastics trigger ferroptosis — a form of iron-dependent cell death driven by fat oxidation — in pig egg cells, disrupting their maturation and reproductive viability. This finding raises concerns about nanoplastic exposure potentially impairing fertility by damaging the eggs needed for reproduction.
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
Researchers found that mice exposed to polystyrene microplastics combined with a common plastic additive (dibutyl phthalate) developed significantly worse allergic asthma symptoms, including increased airway inflammation driven by a specific type of immune response. The microplastics triggered a form of cell death called ferroptosis in lung cells, which amplified the allergic reaction. Treatment with an iron-binding drug provided relief, suggesting potential therapeutic approaches for people with asthma who are exposed to plastic pollution.
Polystyrene Microplastics Induce Radiotherapy Resistance in Lung Cancer by Suppressing Ferroptosis Through NF-κB Activation
Researchers found that polystyrene microplastics impaired radiotherapy efficacy in lung cancer cells by suppressing ferroptosis—a form of iron-dependent cell death—through NF-κB activation, providing the first evidence that microplastics may contribute to cancer therapy resistance.
Mechanismof S‑Palmitoylationin Polystyrene Nanoplastics-Induced Macrophage Cuproptosis Contributingto Emphysema through Alveolar Epithelial Cell Pyroptosis
Researchers identified S-palmitoylation—a lipid modification process—as a key mechanism by which inhaled polystyrene nanoplastics trigger macrophage ferroptosis (iron-dependent cell death) in the lungs, providing a molecular explanation for how respiratory nanoplastic exposure damages immune cells.
Inhibiting ferroptosis in brain microvascular endothelial cells: A potential strategy to mitigate polystyrene nanoplastics‒induced blood‒brain barrier dysfunction
Researchers found that polystyrene nanoplastics disrupt the blood-brain barrier in mice by triggering ferroptosis — an iron-dependent form of cell death — in brain microvascular endothelial cells, and that blocking ferroptosis with a targeted drug reduced tight junction protein loss and restored barrier integrity.
Chronic exposure to polystyrene microplastics induces renal fibrosis via ferroptosis
Mice exposed to polystyrene microplastics in their drinking water for six months developed kidney scarring (fibrosis) driven by a type of cell death called ferroptosis. The microplastics triggered iron-dependent damage in kidney cells, which then released signals causing surrounding tissue to scar over. This long-term study reveals a new mechanism by which chronic microplastic exposure could lead to progressive kidney disease in humans.
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.
The interplay of ferroptosis and oxidative stress in pulmonary fibrosis: from mechanisms to treatment
This research review summarizes how a specific type of cell death called ferroptosis may contribute to pulmonary fibrosis, a serious lung disease where scar tissue builds up and makes breathing difficult. Scientists have found that when cells die from iron buildup and damage from harmful molecules, it can worsen lung scarring, but drugs that block this process show promise in animal studies. Understanding this connection could lead to new treatments for people with pulmonary fibrosis, though more research is needed to make sure these potential medicines are safe and effective in humans.
Mechanism of S-Palmitoylation in Polystyrene Nanoplastics-Induced Macrophage Cuproptosis Contributing to Emphysema through Alveolar Epithelial Cell Pyroptosis
Researchers found that breathing in polystyrene nanoplastics caused emphysema (a type of lung disease) in rats by triggering a chain reaction: the nanoplastics entered immune cells in the lungs, caused copper-related cell death in those immune cells, which then released inflammatory signals that destroyed the air sacs. This newly discovered mechanism shows how inhaled nanoplastics could contribute to serious, irreversible lung damage.