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Molecular Mechanisms of Phthalates in Depression: An Analysis Based on Network Toxicology and Molecular Docking
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This analysis investigates the molecular pathways through which phthalate exposure may contribute to depression, including effects on hormone signaling, neuroinflammation, and oxidative stress. Phthalates are ubiquitous plasticizers found in food packaging, personal care products, and medical devices, leading to near-universal human exposure. The findings suggest a biologically plausible link between phthalate burden and mental health outcomes, warranting further epidemiological study.
This study investigated the molecular mechanisms by which phthalates induce depression, utilizing network toxicology and molecular docking techniques. By integrating the TargetNet, GeneCards, and PharmMapper databases, 658 potential target genes of phthalates were identified. Additionally, 5433 depression-related targets were retrieved from the GeneCards and OMIM databases. Comparative analysis revealed 360 common targets implicated in both phthalate action and depression. A Protein-Protein Interaction (PPI) network was constructed using the STRING database. Subsequently, the CytoHubba plugin (employing the MCC algorithm) within Cytoscape was used to screen the network, identifying the top 20 hub genes. These core genes include AKT1, CASP3, TNF, TP53, BCL2, and IL6, among others. Validation on the GEO dataset (GSE23848) revealed that the expression of multiple core genes was significantly upregulated in patients with depression (p < 0.05). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses indicated that phthalates mainly regulate biological processes such as extracellular stimulus response, lipopolysaccharide metabolism, and chemical synaptic transmission. Depression is mediated by the AGE-RAGE signaling pathway (a complication of diabetes), lipids and atherosclerosis, Endocrine resistance, and the PI3K-Akt signaling pathway. Molecular docking confirmed that phthalates have strong binding activity with key targets (CASP3, TNF, TP53, BCL2, IL6). These findings present a novel paradigm for evaluating the health risks posed by environmental pollutants.
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This study used network toxicology and molecular docking to investigate how the common plasticizer DEHP (di-(2-ethylhexyl) phthalate) may contribute to metabolic syndrome, identifying key molecular targets and pathways through which DEHP exposure could exacerbate metabolic dysfunction, though experimental validation of these mechanistic findings remains needed.
Computer-Aided Molecular Design Meets Network Toxicology and Molecular Docking: A Joint Strategy to Explore Common Molecular Mechanisms of Phthalates on Human Breast Cancer and Structure–Activity Relationship
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This study used network toxicology and molecular docking to identify shared mechanisms by which three common phthalates (DBP, BBP, DEHP) promote breast cancer, finding that all three interact with five key transcription factor-associated genes including TP53 and ESR1. Computer-aided molecular design revealed that alkyl chain length and phenyl groups are critical structural determinants of phthalate binding affinity to these cancer-relevant targets.
The Mechanism of Bisphenol S‐Induced Atherosclerosis Elucidated Based on Network Toxicology, Molecular Docking, and Machine Learning
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Researchers used network toxicology, molecular docking, and machine learning to identify four core protein targets through which bisphenol S (BPS) may promote atherosclerosis, finding that the chemical disrupts glutathione and tyrosine metabolism pathways critical to cardiovascular health.
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.
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Using a toxicogenomics framework, researchers catalogued 6,470 plastic additives and traced molecular pathways connecting 1,287 of them to adverse health outcomes across 27 disease categories. This approach, known as adverse outcome pathway network mapping, reveals how plastic additives may contribute to a broad range of conditions from endocrine disruption to cardiovascular disease. The findings underscore the need to regulate plastic additives not just individually but as a class based on shared mechanisms of harm.
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