ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2025
Impact of Di-(2-Ethylhexyl)-Phthalate on Metabolic Syndrome: Insights from Network Toxicology and Molecular Docking and Dynamics.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed.
- Network Toxicology Reveals the Mechanisms of the Plasticizer Metabolite MECPP in Metabolic Diseases.International journal of molecular sciences · 2026Article
- The effects of nicotine exposure on depression: An integrative analysis combining network toxicology, molecular docking, and Mendelian randomization.Tobacco induced diseases · 2026Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Metabolic syndrome (MetS) is strongly associated with exposure to environmental pollutants, especially endocrine disruptors (EDCs). Di-(2-ethylhexyl)-Phthalate (DEHP), a typical EDC widely found in plastic products, has been shown to interfere with lipid metabolism and insulin signalling. However, the specific molecular mechanism by which it mediates MetS remains unclear. Purpose: This study aimed to systematically investigate the molecular mechanisms underlying the effects of the ubiquitous environmental pollutant DEHP on MetS, thereby providing new insights into the role of environmental toxins in metabolic disorders. Methods: MetS-related disease targets were searched using the GeneCards, OMIM, and TTD databases. DEHP-related targets were obtained from STITCH, SwissTargetPrediction, and ChEMBL. Constructed PPI networks of intersecting targets and visualized and screened core targets in Cytoscape 3.7.1. GO and KEGG pathway analyses were performed using the DAVID database to elucidate biological processes, cellular components, molecular functions, and key pathways ( Results: 150 intersecting targets were identified between DEHP and MetS. The PPI network exhibited core targets, including TP53, ESR1, EGFR, TNF, and IL6. GO analysis showed entries in metabolic processes, transcriptional regulation, and redox reactions. The KEGG pathway showed significant enrichment in AGE-RAGE, FoxO, insulin resistance, and steroid hormone biosynthesis pathways. DEHP showed strong binding affinity to core targets: TP53 (-5.6 kcal/mol), ESR1 (-6.1 kcal/mol), EGFR (-5.4 kcal/mol), and IL6 (-4.8 kcal/mol). Molecular dynamics simulation further verified the results of molecular docking. Conclusion: Our study highlights the interaction between environmental pollutants and metabolic dysfunction. These findings highlight the potential role of DEHP in exacerbating MetS and provide a basis for mitigating its health risks through targeted interventions. Further experimental validation is needed in the future to confirm these mechanistic insights.
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