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Ferroptosis inhibition by ferrostatin-1 attenuates nanoplastic-induced angiogenesis impairment in zebrafish larvae and human microvascular endothelial cells
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In zebrafish larvae and human blood vessel cells grown in the lab, exposure to nanoplastics damaged blood vessel formation and triggered a cell-damage process called ferroptosis, marked by harmful fat breakdown and reduced protective enzymes. A drug called ferrostatin-1 that blocks ferroptosis reversed these vessel problems in both the zebrafish and the cells.
Nanoplastics (NPs) are widespread environmental pollutants, and their potential cardiovascular toxicity has raised growing concern. This study aimed to investigate whether NPs impair angiogenesis through ferroptosis induction. Zebrafish larvae were exposed to NPs (10-1000 μg/L) or erastin (5 μM) for 48 h. Rescue experiments were performed by co-treatment with ferrostatin-1 (Fer-1, 1 μM). Human microvascular endothelial cell line-1 were treated with NPs at 100 μg/mL for 24 h, with or without Fer-1 (1 μM). NPs exposure resulted in reduced body length, impaired intersegmental vessel formation, and downregulated expression of key angiogenesis-related genes in zebrafish larvae. Additionally, NPs inhibited tube formation, migration, and vascular endothelial growth factor A expression in HMEC-1 cells. Transcriptomic and metabolomic analyses revealed that NPs exposure disrupted unsaturated fatty acid metabolism. NPs induced lipid peroxidation, reactive oxygen species accumulation, elevated malondialdehyde levels, and downregulation of glutathione peroxidase 4 expression, all of which were reversed by treatment with the ferroptosis inhibitor Fer-1. Intervention with Fer-1 not only rescued NPs-induced intersegmental vessel defects but also upregulated the expression of angiogenesis-related genes, thereby effectively ameliorating NPs-induced vascular damage. These findings indicate that ferroptosis is a key mechanism underlying NPs-mediated vascular dysfunction.
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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.
Inhibiting ferroptosis in brain microvascular endothelial cells: A potential strategy to mitigate polystyrene nanoplastics‒induced blood‒brain barrier dysfunction
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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.
ROS-driven crosstalk between ferroptosis and necroptosis mediates neurotoxicity induced by maternal exposure to polystyrene nanoplastics in zebrafish
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Adult female zebrafish were exposed to polystyrene nanoplastics for 28 days. The particles passed to their embryos and larvae, which had lower hatching rates, more malformations, reduced movement and fewer neurons in part of the brain. The damage was driven by oxidative stress and two cell-death pathways, and antioxidant treatment partly reversed it.
The mediating role of ferroptosis and mitochondrial dynamics disorder in the aggravation of cardiac injury by polystyrene microplastics
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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.
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.
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