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61,005 resultsShowing papers similar to Exposure of polystyrene nanoplastics led to ferroptosis on cardiomyocytes
ClearFerroptosis 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.
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.
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.
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.
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.
The impact of polystyrene microplastics on cardiomyocytes pyroptosis through NLRP3/Caspase‐1 signaling pathway and oxidative stress in Wistar rats
Researchers exposed rats to polystyrene microplastics at varying doses and examined the effects on heart tissue. They found that microplastic exposure triggered inflammatory cell death and oxidative stress in heart cells through a specific signaling pathway, suggesting that microplastics may pose risks to cardiovascular health.
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.
Polystyrene microplastics-induced cardiotoxicity in chickens via the ROS-driven NF-κB-NLRP3-GSDMD and AMPK-PGC-1α axes
Researchers found that polystyrene microplastics caused serious heart damage in chickens by triggering oxidative stress, inflammation, and disruption of the cells' energy production systems. The microplastics activated inflammatory pathways that led to a type of cell death called pyroptosis and damaged the mitochondria that power heart cells. These findings suggest that microplastic exposure could pose risks to cardiovascular health in animals, with potential implications for understanding heart-related effects in humans.
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.
The mediating role of ferroptosis and mitochondrial dynamics disorder in the aggravation of cardiac injury by polystyrene microplastics
Researchers investigated how polystyrene microplastics worsen heart injury in mice, particularly when combined with the chemotherapy drug doxorubicin. The study found that microplastics aggravated cardiac damage through ferroptosis and mitochondrial dysfunction pathways, and that two protective compounds, Ferrostatin-1 and luteolin, showed potential in mitigating these harmful effects on heart tissue.
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.
Polystyrene nanoplastics induced cardiomyocyte apoptosis and myocardial inflammation in carp by promoting ROS production
Researchers exposed carp to polystyrene nanoplastics of different sizes and found that the particles caused heart muscle cell death and cardiac inflammation. Smaller nanoplastics penetrated deeper into heart tissue and caused more severe damage by promoting the production of reactive oxygen species. The study provides evidence that nanoplastic pollution in aquatic environments can directly harm fish cardiovascular health.
Cardiotoxicity of polystyrene nanoplastics and associated mechanism of myocardial cell injury in mice
Mice exposed to polystyrene nanoplastics for 42 days developed enlarged hearts, thinner heart walls, and weaker heart contractions in a dose-dependent manner. The nanoplastics triggered inflammation and oxidative stress in heart muscle cells through specific signaling pathways. These findings suggest that nanoplastic exposure could contribute to heart disease, including a condition called dilated cardiomyopathy.
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 nanoplastics trigger mitochondrial and metabolic reprogramming in cardiomyocytes: Evidence from integrated transcriptomic and metabolomic analysis
Scientists found that tiny plastic particles called nanoplastics can damage heart cells by disrupting their powerhouses (mitochondria) and reducing their ability to produce energy. When researchers exposed human heart cells and mice to these nanoplastics, they observed weakened heart function and signs of early heart damage. This research suggests that the growing amount of microscopic plastic pollution in our environment could pose previously unknown risks to heart health.
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.
Embryonic exposure of polystyrene nanoplastics affects cardiac development
Researchers found that polystyrene nanoplastics disrupted the development of heart cells grown from human embryonic stem cells, producing smaller and weaker heart tissue in the lab. The nanoplastics caused oxidative stress in mitochondria and blocked important cellular cleanup processes, reducing the stem cells' ability to properly form heart cells. In zebrafish embryos, nanoplastic exposure also reduced heart contractions and blood flow, suggesting that nanoplastic exposure during pregnancy could pose risks to fetal heart development.
Dissection of the potential mechanism of polystyrene microplastic exposure on cardiomyocytes
Researchers investigated how polystyrene microplastics affect human heart muscle cells at concentrations reflecting estimated daily human intake levels. They found that the microplastics caused oxidative stress, mitochondrial dysfunction, and disrupted calcium signaling in the cells. The study suggests that microplastic exposure may contribute to cardiovascular risks by directly damaging heart cell function at the cellular level.
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.
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.
Activation of pyroptosis and ferroptosis is involved in the hepatotoxicity induced by polystyrene microplastics in mice
Researchers exposed mice to polystyrene microplastics and found that the particles caused significant liver damage, including structural changes and impaired function. The study identified two specific cell death pathways, pyroptosis and ferroptosis, as key mechanisms driving the liver injury. These findings suggest that microplastic exposure may harm liver health through multiple biological pathways that warrant further investigation.
Polystyrene nanoplastics trigger ferroptosis in Nrf2-deficient gut via ether phospholipid accumulation
Researchers discovered that polystyrene nanoplastics trigger a specific type of cell death called ferroptosis in gut lining cells by disrupting fat metabolism, and that mice lacking a key protective protein (Nrf2) in their intestines were especially vulnerable. A high-fat diet made the damage worse, suggesting that people with poor diets or reduced antioxidant defenses may be at greater risk of intestinal harm from nanoplastic exposure.
Polystyrene microplastics cause cardiac fibrosis by activating Wnt/β-catenin signaling pathway and promoting cardiomyocyte apoptosis in rats
Researchers exposed rats to polystyrene microplastics at varying concentrations for 90 days and examined cardiovascular effects. The study found that microplastic exposure activated the Wnt/beta-catenin signaling pathway and promoted cardiomyocyte apoptosis, leading to cardiac fibrosis, suggesting that chronic microplastic exposure may pose risks to cardiovascular health.