ArticleToxicology research2024
Predicting the molecular mechanisms of cardiovascular toxicity induced by per- and polyfluoroalkyl substances: an In Silico network toxicology perspective.
Article in Toxicology research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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Who cites it
4 citing papers in PubMed.
- Imaging and Molecular Biomarkers of PFAS-Related Vascular Aging: A Narrative Review.International journal of molecular sciences · 2026Review
- Activation of the Nrf2/ARE Pathway Attenuates BDE-47-Induced Immunotoxicity in RAW264.7 Macrophages.Biomolecules · 2026Article
- Mechanistic insights into PFAS derivatives-induced coronary heart disease and atherosclerotic renal artery stenosis via integrated network toxicology and molecular modeling.Toxicology research · 2026Article
- Mechanistic Analysis of Decabromodiphenyl Ether-Induced Neurotoxicity in Humans Using Network Toxicology and Molecular Docking.Neurotoxicity research · 2025Article
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
backgroundPer- and polyfluoroalkyl substances (PFAS) are human-made chemicals that accumulate in the human body and the environment over time. Humans are primarily exposed to PFAS through drinking water, food, consumer products, and dust. These exposures can have many adverse health effects, including cardiovascular diseases (CVDs) and factors contributing to CVDs. This study identified the molecular mechanisms of CVDs caused by PFAS.
methodsFor this purpose, various computational tools, such as the Comparative Toxicogenomic Database, ShinyGO, ChEA3, MIENTURNET, GeneMANIA, STRING, and Cytoscape, were used to conduct in silico analyses.
resultsThe results showed that 10 genes were common between PFAS and CVDs, and among these common genes, the PPAR signaling pathway, fatty acid metabolic processes, and lipid binding were the most significantly associated gene ontology terms. Among the top 10 transcription factors (TFs) related to these common genes, peroxisome proliferator-activated receptor gamma and androgen receptor were the most prominent. Additionally, hsa-miR-130b-3p, hsa-miR-130a-3p, and hsa-miR-129-5p were featured microRNAs involved in PFAS-induced CVDs. Finally,
conclusionThese findings may contribute to a better understanding of the molecular mechanisms and reveal new potential targets in PFAS-induced CVDs.
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