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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
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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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Researchers used network toxicology, molecular docking, and machine learning to identify how PET microplastics may promote atherosclerosis, narrowing 28 candidate targets to seven key genes and predicting interactions with atherosclerosis-relevant pathways including inflammation and lipid metabolism.
Mechanistic Insights into PET-MPs-Aggravated Ischemic Stroke via Integrated Computational–Experimental Approaches
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Scientists found that PET microplastics—tiny plastic particles from common plastic bottles and packaging that have been detected in human brains—can make strokes worse by increasing inflammation and cell damage in the brain, based on tests in mice and lab-grown cells. This matters because it suggests everyday plastic pollution exposure could be an added risk factor for stroke severity, though more research is needed to confirm this happens the same way in humans.
Mechanistic Insights into PET-MPs-Aggravated Ischemic Stroke via Integrated Computational–Experimental Approaches
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Scientists found that tiny plastic particles called PET microplastics—common pollutants that can end up in our bodies, including the brain—made strokes worse in mice by increasing brain inflammation and cell damage. Using a mix of computer modeling and lab experiments, they pinpointed specific biological pathways that explain how these plastics harm the brain during a stroke. While this study was done in mice and cells, not humans, it adds to growing evidence that everyday plastic pollution could be a hidden risk factor for serious health conditions like stroke.
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