We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Papers
61,005 resultsShowing papers similar to The interplay of ferroptosis and oxidative stress in pulmonary fibrosis: from mechanisms to treatment
ClearFerritinophagy 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.
Targeting Regulated Cell Death Pathways in COPD: Mechanisms and Therapeutic Strategies
This review examines how multiple regulated cell death pathways — including apoptosis, necroptosis, pyroptosis, ferroptosis, and autophagy — contribute to chronic obstructive pulmonary disease progression and discusses these pathways as potential therapeutic targets.
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.
Ferroptosis of smooth muscle cells in vascular diseases: from basic principles to clinical translation
Scientists have discovered that smooth muscle cells in blood vessels can die through a process called "ferroptosis" - a type of cell death caused by iron buildup and toxic fats. This review of existing research shows that this cell death process contributes to many serious heart and blood vessel diseases, including atherosclerosis, high blood pressure, and aneurysms. Understanding how this happens could lead to new treatments that protect blood vessels and reduce the risk of heart attacks and strokes.
Targeting GSTP1-dependent ferroptosis in lung cancer radiotherapy: Existing evidence and future directions
This review explores the relationship between the protein GSTP1, ferroptosis (a form of iron-dependent cell death), and radiotherapy resistance in lung cancer. Researchers propose that targeting GSTP1 could help overcome tumor cell resistance to radiation by promoting ferroptosis. While focused on cancer treatment mechanisms, the study touches on how environmental factors and oxidative stress pathways relevant to pollutant exposure intersect with cellular defense mechanisms.
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 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 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.
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.
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.
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.
Interaction of ferroptosis and cuproptosis in the perspective of pulmonary hypertension
This review examines how disruptions in copper and iron metabolism, through mechanisms called cuproptosis and ferroptosis, may contribute to pulmonary hypertension. While not directly focused on microplastics, the study explores how environmental factors that disrupt metal homeostasis can drive disease through oxidative stress and mitochondrial dysfunction, pathways that are also relevant to understanding how environmental contaminants affect human health.
International consensus guidelines for the definition, detection, and interpretation of autophagy-dependent ferroptosis
This scientific review provides guidelines for understanding a specific type of cell death called autophagy-dependent ferroptosis, where cells essentially digest their own protective components and then die from iron-driven damage. While not directly about microplastics, this process is relevant because microplastics and nanoplastics have been shown to trigger oxidative stress and iron-related cell damage in tissues. Understanding these cell death pathways helps researchers assess how plastic particle exposure could harm organs like the liver, brain, and lungs.
Redox Biology and Liver Fibrosis
This review explores how disrupted redox balance in the liver contributes to the development and progression of hepatic fibrosis across various chronic liver diseases. Researchers describe how persistent damage to liver cells triggers overproduction of reactive species, which in turn activate specific signaling pathways that drive scar tissue formation. The study identifies several redox-dependent pathways as potential therapeutic targets for slowing or preventing liver fibrosis.
Coal dust nanoparticles induced pulmonary fibrosis by promoting inflammation and epithelial-mesenchymal transition via the NF-κB/NLRP3 pathway driven by IGF1/ROS-mediated AKT/GSK3β signals
Researchers investigated how coal dust nanoparticles trigger lung scarring (pulmonary fibrosis) in coal miners, identifying a molecular chain reaction where nanoparticles activate the IGF1 signaling pathway, generate damaging reactive oxygen species, and ultimately drive inflammation and tissue remodeling. The study pinpoints specific drug targets that could potentially prevent or treat the lung disease that affects millions of miners worldwide.
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.
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.
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.
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.
Research progress on ferroptosis in the pathogenesis and treatment of neurodegenerative diseases
This review explores ferroptosis, a type of iron-dependent cell death that damages brain cells through fat oxidation, and its role in neurodegenerative diseases like Alzheimer's and Parkinson's. While not directly about microplastics, ferroptosis is one of the cellular damage pathways that microplastic exposure can trigger in brain tissue. Understanding how ferroptosis works may help explain how environmental pollutants, including nanoplastics that can cross the blood-brain barrier, contribute to neurological damage.
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.
Ferroptosis: First evidence in premature duck ovary induced by polyvinyl chloride microplastics
Researchers discovered that polyvinyl chloride microplastics caused premature ovarian damage in ducks through a cell death process called ferroptosis, which involves iron-dependent oxidative damage. Higher microplastic concentrations led to iron accumulation, increased oxidative stress, and structural damage to ovarian tissue. This is the first evidence linking microplastic exposure to ferroptosis in the avian reproductive system.
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.