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61,005 resultsShowing papers similar to Microplastic exposure induces preeclampsia-like symptoms via HIF-1α/TFRC-mediated ferroptosis in placental trophoblast cells
ClearPolystyrene Nanoplastics induced placental toxicology by activating Keap1-mediated ferroptosis via METTL3-dependent m6A methylation
Scientists found that tiny plastic particles called nanoplastics can damage the placenta during pregnancy by triggering a harmful process called ferroptosis, which kills cells through iron buildup. The study used lab cells and pregnant mice to show how these plastic particles disrupt the body's natural protective systems in placental tissue. This research helps explain why microplastics in our environment might pose risks during pregnancy, though more studies are needed to understand the full impact on human health.
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.
Polystyrene nanoparticles induced adverse pregnancy outcomes via the activation of placental ferroptosis and gut microbiota dysfunction
Researchers exposed pregnant mice to 50-nanometer polystyrene nanoparticles and found that the particles caused adverse pregnancy outcomes through two interconnected mechanisms: disruption of gut microbiota and activation of ferroptosis in placental tissue. The nanoparticle exposure altered the composition of beneficial gut bacteria and triggered iron-dependent cell death in the placenta. The study suggests that maternal exposure to nanoplastics during pregnancy may threaten reproductive health through gut-placenta axis disruption.
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.
Microplastics caused embryonic growth retardation and placental dysfunction in pregnant mice by activating GRP78/IRE1α/JNK axis induced apoptosis and endoplasmic reticulum stress
When pregnant mice were fed polystyrene microplastics, their embryos showed growth delays and their placentas were damaged through a specific stress pathway involving the endoplasmic reticulum, the cell's protein-processing center. These findings suggest that microplastic exposure during pregnancy could interfere with fetal development by triggering cell death in placental tissue.
Adverse effects of a realistic concentration of human exposure to microplastics on markers of placental barrier permeability in pregnant rats
Researchers exposed pregnant rats to polystyrene microplastics at concentrations realistic for human exposure and examined effects on the placenta. They found that the microplastics accumulated in placental tissue, caused oxidative stress, triggered cell death, and reduced the expression of proteins that maintain the placental barrier. The study provides the first evidence that realistic levels of microplastic exposure can compromise the protective barrier between mother and developing offspring.
Maternal exposure to polystyrene microplastics alters placental metabolism in mice
Researchers exposed pregnant mice to polystyrene microplastics and examined how placental metabolism was affected. The study found significant changes in placental metabolic pathways that could help explain the fetal growth restriction previously observed in microplastic-exposed pregnancies. These findings suggest that microplastic exposure during pregnancy may interfere with the placenta's ability to support normal fetal development.
Polystyrene microplastics induce biochemical and metabolism changes in human placental explants
Researchers investigated the effects of polystyrene microplastics on human placental cells, finding that exposure altered biochemical pathways and metabolic activity. The results suggest that microplastics reaching the placenta can disrupt cellular functions important for fetal development.
Polystyrene microplastics induce biochemical and metabolism changes in human placental explants
This study examined how polystyrene microplastics affect biochemical pathways and metabolism in human placental cells, with microplastics having been detected in human placental tissue. Polystyrene microplastics induced metabolic and biochemical changes in placental cells, raising concern for placental function and fetal health during pregnancy.
Gestational exposure to micro- and nanoplastics leads to poor pregnancy outcomes by impairing placental trophoblast syncytialization
Researchers found that exposing pregnant mice to micro- and nanoplastics led to increased embryo loss, reduced embryonic weight, and smaller placentas. The plastic particles impaired a critical process called syncytialization, where placental cells fuse together to form a functional barrier, by activating a stress-response signaling pathway. The study suggests that prenatal microplastic exposure could disrupt placental development and contribute to poor pregnancy outcomes.
PS-MPs or their co-exposure with cadmium impair male reproductive function through the miR-199a-5p/HIF-1α-mediated ferroptosis pathway
Researchers found that polystyrene microplastics, especially when combined with cadmium, caused significant reproductive damage in male mice through a cell death pathway called ferroptosis. Smaller microplastic particles were more toxic than larger ones, and the combination of microplastics with cadmium amplified the harm beyond what either caused alone. The study identifies a specific molecular mechanism by which microplastics and heavy metals together may threaten male reproductive health.
Microplastic exposure in daily life and the risk of pregnancy-induced hypertension: A study on the association between environmental pollutants and maternal-fetal health outcomes
In a study of pregnant women, those with pregnancy-induced high blood pressure had 1.46 times more microplastics in their umbilical cords than healthy pregnant women, with polyethylene and polycarbonate being especially elevated. Microplastic exposure was linked to use of plastic containers and takeout meals, and higher levels were associated with worse outcomes for newborns. While this preliminary study has limitations, it suggests that everyday microplastic exposure during pregnancy may be connected to dangerous blood pressure complications.
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.
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 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.
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.
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.
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.
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.
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 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.
HIF-1α/HO-1-Mediated Ferroptosis Participates in Polystyrene Nanoplastics-Induced Intergenerational Cardiotoxicity
When pregnant mice were exposed to polystyrene nanoplastics, the particles crossed into offspring hearts and caused heart damage through a process called ferroptosis, a type of iron-dependent cell death. The nanoplastics activated a specific molecular pathway involving HIF-1 alpha and HO-1 that led to iron buildup, mitochondrial injury, and oxidative stress in heart tissue. This study raises concerns that maternal nanoplastic exposure during pregnancy could harm fetal heart development in ways that may have lasting consequences.
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.
Polystyrene microplastics disturb maternal glucose homeostasis and induce adverse pregnancy outcomes
Pregnant mice exposed to polystyrene microplastics developed abnormal blood sugar levels and experienced poor pregnancy outcomes, including placental damage and restricted fetal growth. The study found that microplastics disrupted glucose metabolism through inflammation and a cellular stress response, suggesting that microplastic exposure during pregnancy could contribute to complications similar to gestational diabetes.