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Environmental pollution is an important risk factor for hypertension, and bisphenol A (BPA) is a prevalent environmental contaminant. This study aimed to investigate the potential toxicity of BPA and the underlying molecular mechanisms of BPA-induced hypertension through network toxicology and molecular docking. Initially, we predicted that BPA would be cardiotoxic. We subsequently identified 51 potential targets and extracted 14 core targets of the effects of BPA on hypertension. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis demonstrated that these core targets were involved primarily in the estrogen signaling pathway and the calcium signaling pathway. Furthermore, molecular docking confirmed the binding capacity of BPA to these core targets, with  ADRB2 ,  ESR1 , and  MMP9  potentially being the key targets through which BPA influences hypertension. Our study elucidates the molecular mechanisms of BPA toxicity and its role in hypertension induction, providing a foundation for the prevention and treatment of hypertension associated with environmental BPA exposure.

Network toxicology and molecular docking strategy for Analyzing the toxicity and mechanisms of Bisphenol a in hypertension