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Exposure of polystyrene nanoplastics led to ferroptosis on cardiomyocytes
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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.
Recent studies have revealed that nanoplastics (nm-sized nanoplastics may induce oxidative stress) can translocate into human cardiovascular tissues and potentially contribute to pathophysiological processes through mechanisms involving reactive oxygen species (ROS) generation. However, the exact role of these materials in inducing iron-related diseases such as ferroptosis remains unclear. In this investigation, we demonstrated that 100 nm polystyrene nanoparticles (PS-NPs) can be taken up by primary rat cardiomyocytes and induce mitochondrial reactive oxygen species (ROS) elevation, mitochondrial membrane potential decrease, ferrrous iron accumulation, and lipid peroxidation. These changes ultimately result in significant reduction of cell viability alongside upregulation of pro-ferroptotic proteins such as COX2, ACSL4, and downregulation of antioxidant proteins like GPX4. Furthermore, ferrous deferoxamine (DFO) effectively restored cellular viability by inhibiting the increase in ferrrous iron and lipid peroxidation. Additionally, autophagy and NF-κB-IL6 signaling pathways were activated in response to PS-NPs exposure. These findings suggest that PS-NPs may serve as a novel agent inducing ferroptosis in cardiomyocytes.
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Exposure to Polystyrene Nanoplastics Induces Ferroptosis-Associated Cardiac Injury: Cell-Based Evidence for Lysosome-Associated NLRX1 Loss and an NLRX1–STING–NCOA4 Response
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In mouse heart cells and in mice given polystyrene nanoplastics by mouth for eight weeks, the particles lowered the proteins NLRX1 and GPX4 and promoted iron buildup and lipid damage. The mice developed cardiac dysfunction and fibrosis.
Ferroptosis involved in inhaled polystyrene microplastics leaded myocardial fibrosis through HIF-ROS-SLC7A11/GPX4 Pathway
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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
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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.
The mechanism of vascular injury caused by polystyrene microplastics: Involving ferroptosis and metabolomics
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Mice exposed to microplastics showed damaged blood vessels, worse cholesterol levels, and a type of cell death called ferroptosis (basically cells dying from oxidative damage). A drug that blocked this cell death reduced the vessel damage, hinting that microplastics may harm heart and blood vessel health, though this was shown in mice, not yet confirmed in humans.
HIF-1α/HO-1-Mediated Ferroptosis Participates in Polystyrene Nanoplastics-Induced Intergenerational Cardiotoxicity
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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.
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