ArticleCardiovascular toxicology2026
Integrative Network Pharmacology and Molecular Docking-Based Validation of Berberine as a Therapeutic Agent in Arsenic-Induced Cardiotoxicity.
Article in Cardiovascular toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Pioglitazone Mitigates Arsenic-Induced Cardiotoxicity via Lipid Metabolism: Network Pharmacology and Molecular Docking Approach.Cardiovascular toxicology · 2026Article
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3 authors.
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Abstract
Exposure to arsenic (As) is a serious environmental and public health risk because it can cause systemic toxicity, which could lead to serious cardiovascular disease like heart failure, arrhythmias, and coronary heart disease (CHD). Exploring safer and multi-target therapeutic agents is gaining popularity as a result of the shortcomings of traditional therapies. The isoquinoline alkaloid berberine which is derived from plants, exhibits strong anti-inflammatory, antioxidant, and cardioprotective properties. This study employs an integrated network pharmacology and molecular docking approach to investigate the molecular mechanisms and therapeutic potential of berberine in arsenic-induced cardiotoxicity. Key genes target arsenic-induced cardiotoxicity and berberine, have been identified using the Swiss Target Prediction, Gene Cards, OMIM, and CTD databases. A protein-protein interaction (PPI) network was generated by analysing frequently intersecting genes with the STRING and Cytoscape tools. Shiny GO was used to conduct pathway enrichment analysis for the KEGG and Gene Ontology databases. Auto Dock was used to assess berberine's binding affinity. Berberine and arsenic-related cardiotoxicity shared 17 common targets. The primary targets were identified using Cytoscape ABL-1 (2G2F), CDK2 (1HCK), CYP19A1 (3EQM), ICAM-1 (4G6J), KIT (1T45), MAPK14 (3PY3), PGR (1A28), PTGS2 (5F19), RAC1 (3TH5), and SRC (2SRC). Enrichment analysis revealed TNF, VEGF, and AGE-RAGE signaling involvement, all of which are linked to oxidative stress, inflammation, and endothelial dysfunction. Binding affinity between berberine and the target was found to be ABL-1 (-9.2 kcal/mol), PTGS2 (-8.8 kcal/mol), SRC (-8.7 kcal/mol), CYP19A1 (-8.6 kcal/mol), KIT (-8.3 kcal/mol), RAC1 (-7.9 kcal/mol), CDK2 (-7.5 kcal/mol), ICAM-1 (-7.2 kcal/mol), MAPK (-6.8 kcal/mol), PGR (-5.6 kcal/mol). Berberine has multi-targeted therapeutic potential for arsenic-induced cardiotoxicity by modulating inflammatory and oxidative pathways. These results could support the possible usage of berberine in the treatment of cardiovascular diseases caused by arsenic and provide a mechanistic link for further experimental validation.
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