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Assessing the toxicological effects of exposure to environmental pollutants PET-MPs on vascular diseases: insights from network toxicology, molecular docking, molecular dynamics, and experimental validation
Summary
Researchers used network toxicology, molecular docking, and cell experiments to investigate how PET microplastics may contribute to vascular diseases. They identified four core molecular targets and found that PET microplastics induced mitochondrial oxidative stress, increased reactive oxygen species, and promoted vascular smooth muscle cell death. The study provides initial molecular-level evidence that microplastic exposure may be a contributing factor in vascular damage and remodeling.
Polyethylene terephthalate microplastics (PET-MPs) pose significant environmental and health concerns due to their persistence and potential toxicity. However, their impact on vascular diseases, especially atherosclerosis (AS), abdominal aortic aneurysm (AAA), and vascular remodeling, is still poorly understood. This study systematically explored the molecular mechanisms of PET-MP-induced vascular toxicity through bioinformatic analysis and experimental validation. Several databases, including GEO, DisGeNET, TargetNet, and SupPred, were used to identify potential molecular targets, with STRING and Cytoscape employed for further core target analysis. GO and KEGG pathway analyses via the DAVID database, complemented by molecular docking and dynamics simulations, validated key interactions.The bioinformatic analysis highlighted four core targets: AKT1, TNF, Caspase3, and VCAM1, and implicated PET-MPs in C-type lectin receptor signaling, AGE-RAGE signaling, and apoptosis pathways.In vitro experiments revealed that PET-MPs induced mitochondrial oxidative stress, reduced mitochondrial membrane potential, increased ROS production, and promoted VSMC apoptosis, thereby contributing to vascular remodeling.
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