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61,005 resultsShowing papers similar to Double-edged Sword Role of Iron-loaded Ferritin in Extracellular Vesicles
ClearFerroptosis 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 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.
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.
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.
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.
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.
Co-exposure of arsenic and polystyrene-nanoplastics induced kidney injury by disrupting mitochondrial homeostasis and mtROS-mediated ferritinophagy and ferroptosis
Researchers found that arsenic and polystyrene nanoplastics together — but not separately — cause kidney fibrosis in mice by disrupting mitochondrial function and triggering a form of iron-dependent cell death called ferroptosis, with mitochondria-targeted antioxidants significantly reducing the combined damage.
Unraveling the impact of nanoplastics on bone microenvironment: focus on extracellular vesicle-mediated communication and oxidative stress in multiple myeloma.
This study reviewed how nanoplastic particles disrupt the bone microenvironment through oxidative stress and damage to the extracellular matrix. Reactive oxygen species generated by nanoplastic exposure were found to drive toxicity in bone cells.
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.
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.
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 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.
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.
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.
Gestational exposure to nanoplastics disrupts fetal development by promoting the placental aging via ferroptosis of syncytiotrophoblast
This mouse study found that exposure to nanoplastics during pregnancy caused placental aging and fetal growth restriction through a process called ferroptosis -- a type of iron-dependent cell death -- in the cells that form the barrier between mother and baby. When researchers blocked the ferroptosis process, fetal weight improved, suggesting this pathway could be a target for protecting pregnancies from nanoplastic-related harm.
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.
Iron's silent betrayal: Ferritinophagy-driven mitochondrial damage mediates polylactic acid nanoplastics and Cr(VI)-induced cardiac injury
Researchers found that co-exposure of mice to biodegradable polylactic acid nanoplastics and hexavalent chromium causes synergistic cardiac injury by inducing ferritinophagy — a process where cells break down iron-storage proteins — triggering iron overload and excess mitochondrial reactive oxygen species that damage heart tissue.
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.
Oridonin-induced ferroptosis and apoptosis: a dual approach to suppress the growth of osteosarcoma cell
This study investigated the anti-tumor effects of oridonin, a natural plant compound, on osteosarcoma cells, finding it triggered both ferroptosis and apoptosis to suppress tumor growth. While focused on cancer treatment rather than microplastics, the ferroptosis pathway studied is also implicated in cellular damage caused by microplastic exposure.
Unraveling the impact of nanoplastics on bone microenvironment: focus on extracellular vesicle-mediated communication and oxidative stress in multiple myeloma.
Researchers reviewed how nanoplastics affect the bone microenvironment, focusing on oxidative stress pathways and extracellular matrix disruption as key mechanisms of toxicity. Reactive oxygen species generated by nanoplastic exposure were identified as drivers of bone cell damage.
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.
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.
Iron Oxide Nanoparticles: Selectively Targeting Melanoma Cells In Vitro by Inducing DNA Damage via H2AX Phosphorylation and Hindering Proliferation through ERK Dephosphorylation
Researchers investigated iron oxide magnetic nanoparticles and found they selectively target melanoma cancer cells while sparing healthy skin cells. The nanoparticles triggered DNA damage and blocked cell growth signals specifically in melanoma cells, and their effectiveness was further enhanced using magnetic heating. The study explores a nanotechnology-based approach to cancer treatment rather than microplastic-related research.
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.