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Evaluating the toxicological effects of PET-MPs exposure on atherosclerosis through integrated network toxicology analysis and experimental validation
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Researchers used network toxicology analysis and laboratory experiments to investigate how polyethylene terephthalate microplastics may contribute to atherosclerosis. They identified several molecular targets and biological pathways through which these microplastics could promote plaque formation in blood vessels. The study provides preliminary evidence that a commonly encountered type of microplastic may interact with cardiovascular disease mechanisms, though further research is needed to confirm these findings.
Polyethylene terephthalate microplastics (PET-MPs) can enter the human body and accumulate through various pathways. However, the toxicological mechanism by which they cause atherosclerosis (AS) remains unclear. PET targets from the ChEMBL, SwissTargetPrediction, SEA, and PharmMapper databases; AS targets from the GeneCards and OMIM databases; and RNA-seq data related to AS were retrieved from the GEO database. The intersection of the aforementioned targets was taken to identify the potential targets of PET-induced AS. Enrichment analysis was conducted on these intersecting genes. The protein-protein interaction (PPI) network was used to further screen the core targets. Single-cell RNA sequencing data of atherosclerotic tissues were retrieved from the GEO database. Molecular docking was carried out using the AutoDock Vina software. Cell experiments were conducted using kit-based detection and PCR technology. A total of 41 potential targets of PET-induced AS were obtained. After further screening, four core targets were obtained, namely CCL5, CTSB, PPARG, and TNF. The expression of core target genes exhibited cellular heterogeneity in atherosclerotic plaque tissues. Enrichment analysis indicated that PET might induce AS through multiple signaling pathways. The results of molecular docking indicated that PET had a certain affinity for all four core target proteins. Cell experiments showed that PET-MPs may exacerbate AS by promoting inflammatory responses. In this study, we use a combination of bioinformatics and experimental verification to initially explore the potential toxicological mechanism by which PET-MPs induce AS.
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