ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Evaluating the toxicological effects of PET-MPs exposure on atherosclerosis through integrated network toxicology analysis and experimental validation.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Emerging cardiovascular risks of micro- and nanoplastics: toxic effects and mechanistic pathways.Particle and fibre toxicology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
Identifiers
41540215What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.