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61,005 resultsShowing papers similar to Ferroptosis of smooth muscle cells in vascular diseases: from basic principles to clinical translation
ClearThe 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.
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.
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.
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.
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.
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.
Potential application of traditional Chinese medicine in cerebral ischemia—Focusing on ferroptosis
This review examined evidence for traditional Chinese medicine compounds in treating cerebral ischemia by targeting ferroptosis, an iron-dependent form of regulated cell death. Multiple TCM-derived compounds including flavonoids and alkaloids showed neuroprotective effects through ferroptosis pathway inhibition in experimental ischemia models.
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.
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.
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.
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.
Ferroptosis inhibition via the ROS-GPX4 axis drives microplastic-induced malignant progression of nasopharyngeal carcinoma
Researchers investigated how polystyrene microplastics promote malignant progression in nasopharyngeal carcinoma cells, finding that the plastics inhibit ferroptosis—an iron-dependent cell death pathway—via the ROS-GPX4 axis, thus allowing cancer cells to survive and proliferate. Blocking this anti-ferroptosis effect restored cancer cell death, suggesting that targeting the ferroptosis pathway could counteract microplastic-driven tumor progression.
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: 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.
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.
Research Progress on Micro(nano)plastic-Induced Programmed Cell Death Associated with Disease Risks
This review summarizes how micro and nanoplastics can trigger different types of programmed cell death, including ferroptosis, pyroptosis, and apoptosis, based on recent animal and cell studies. These forms of cell death are linked to inflammation and diseases affecting the gut, liver, lungs, brain, and reproductive system. The findings help explain the biological mechanisms through which microplastic exposure could contribute to chronic disease in humans.
Double-edged Sword Role of Iron-loaded Ferritin in Extracellular Vesicles
This review explores the dual role of iron-loaded ferritin in extracellular vesicles, discussing how excess cellular iron promotes Fenton reaction-driven oxidative DNA damage and cellular ferroptosis resistance, contributing to carcinogenesis.
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.
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.
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.
An Emerging Role of Micro- and Nanoplastics in Vascular Diseases
This review summarizes emerging research on how micro- and nanoplastics may contribute to vascular diseases, which are the leading cause of death worldwide. Studies suggest that these tiny plastic particles can damage blood vessel walls, promote inflammation, and worsen conditions like atherosclerosis. While more research is needed, the evidence points to microplastic exposure as a potential new risk factor for heart and blood vessel diseases.
Interplay of Ferroptosis, Cuproptosis, Autophagy and Pyroptosis in Male Infertility: Molecular Crossroads and Therapeutic Opportunities
This review examines how different types of cell death, including ferroptosis, cuproptosis, pyroptosis, and autophagy, contribute to male infertility by damaging sperm-producing cells. Environmental toxins, including microplastics, can trigger these destructive pathways through oxidative stress and mitochondrial damage. Understanding these mechanisms is important because it helps explain how environmental pollutant exposure could be contributing to declining male fertility worldwide.
Microplastics induced inflammation and apoptosis via ferroptosis and the NF-κB pathway in carp
Researchers exposed carp to polyethylene microplastics and found they caused serious intestinal damage through two harmful pathways: ferroptosis (a type of iron-dependent cell death) and NF-kB-driven inflammation. The microplastics triggered a buildup of iron and reactive oxygen species in gut tissue, leading to cell death and tissue destruction. Since humans also ingest microplastics that reach the gut, these findings highlight a potential mechanism by which microplastics could damage our digestive system.
Xenoferroptosis, a double-hit challenge for regulated cell death
This review explored xenoferroptosis—a form of regulated cell death driven by iron-dependent lipid peroxidation triggered by environmental contaminants including microplastics and heavy metals. The authors found that xenoferroptosis represents a double-hit mechanism linking environmental exposure to neurodegenerative diseases like Alzheimer's and Parkinson's.