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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.
The increasing prevalence of environmental pollutants has raised public concern about their potential role in diseases such as atherosclerosis (AS). Existing studies suggest that chemicals, including bisphenol S (BPS), may adversely affect cardiovascular health, but the specific mechanisms remain unclear. This study aims to elucidate the effects of BPS on AS and the underlying mechanisms. Through an extensive search of databases such as ChEMBL, STITCH, SwissTargetPrediction, SuperPred, SEA, and GEO, we identified 34 potential targets related to BPS-induced AS. A target network was constructed using the STRING platform and Cytoscape software. GO and KEGG functional enrichment analysis using the DAVID database revealed that BPS may promote the occurrence of AS by interfering with critical biological processes such as glutathione metabolism, nitrogen metabolism, and tyrosine metabolism. This was followed by the selection of 4 core targets-aminopeptidase n (ANPEP), alcohol dehydrogenase 5 (ADH5), lysosomal pro-x carboxypeptidase (PRCP), and microsomal glutathione s-transferase 1 (MGST1)-using five machine learning methods. These core targets play a pivotal role in BPS-induced AS. Furthermore, molecular docking confirmed the tight binding between BPS and these core targets. In conclusion, this study provides a theoretical framework for understanding the molecular mechanisms of BPS-induced AS and contributes scientific evidence for the development of prevention and treatment strategies for cardiovascular diseases triggered by BPS exposure.
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Scientists found that PET microplastics—tiny plastic particles from common plastic bottles and packaging that have been detected in human brains—can make strokes worse by increasing inflammation and cell damage in the brain, based on tests in mice and lab-grown cells. This matters because it suggests everyday plastic pollution exposure could be an added risk factor for stroke severity, though more research is needed to confirm this happens the same way in humans.
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Scientists found that tiny plastic particles called PET microplastics—common pollutants that can end up in our bodies, including the brain—made strokes worse in mice by increasing brain inflammation and cell damage. Using a mix of computer modeling and lab experiments, they pinpointed specific biological pathways that explain how these plastics harm the brain during a stroke. While this study was done in mice and cells, not humans, it adds to growing evidence that everyday plastic pollution could be a hidden risk factor for serious health conditions like stroke.
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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