Exploring the Mechanisms of EDCs-Induced Metabolic Disorders in Humans Using Network Toxicology and Molecular Docking.

OBJECTIVE

This study aims to investigate the potential mechanisms by which EDCs, recognized as emerging pollutants, induce metabolic disorders leading to metabolic diseases in humans.

METHODS

Network toxicology and molecular docking techniques were employed to elucidate the molecular mechanisms underlying EDCs-induced pathogenesis of the six diseases. Potential targets associated with EDCs and these diseases were identified using databases such as PubChem, ChEMBL, Super-PRED, GeneCards, OMIM, and TTD. STRING analysis and Cytoscape software were further utilized to determine core targets most significantly linked to these metabolic disorders. GO and KEGG pathway enrichment analyses were performed on the core targets using the DAVID database. Finally, molecular docking was conducted to validate the binding affinities between EDCs and core target proteins.

RESULTS

EDCs may potentially induce metabolic disorders by modulating cellular expression, influencing apoptosis and proliferation, and regulating related signaling pathways. Notably, a close interrelationship was observed among lipid metabolism disorders and atherosclerosis, Alzheimer's disease, type 2 diabetes mellitus, osteoporosis, hyperuricemia, and non-alcoholic fatty liver disease.

CONCLUSION

This study provides novel insights into the mechanisms through which EDCs induce metabolic diseases in humans and highlights correlations among distinct disorders, thereby establishing a theoretical foundation for disease prevention and therapeutic strategies.