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Background <p>Previous studies have shown that chemicals produced by the combustion of carbon-containing fuels, such as benzo[a]pyrene (BaP), can adversely affect chronic degenerative diseases, including cataracts. However, the molecular mechanisms underlying BaP’s role in cataract development and progression remain unclear.</p> Objective <p>This study aimed to explore the potential molecular mechanisms by which BaP contributes to the onset and progression of cataracts.</p> Results <p>By systematically analyzing databases such as ChEMBL and STITCH, we identified 57 potential targets closely related to both BaP and cataracts. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses revealed that these targets are primarily involved in mitochondrial function, cellular energy metabolism, and redox reactions. Protein–protein interaction (PPI) network analysis identified three core targets: CCR7, CCR9, and CCL22. Molecular docking demonstrated stable binding between BaP and these core proteins, suggesting their key roles in BaP-induced lens toxicity. Immune infiltration analysis indicated that the expression of these hub genes was closely associated with the abundance of various immune cell types in cataract tissues. Furthermore, ssGSEA showed significant differences in the infiltration levels of activated B cells, activated CD4 T cells, activated CD8 T cells, and regulatory T cells between groups stratified by hub gene expression. Finally, a nomogram model based on these hub genes exhibited high diagnostic accuracy for cataracts (AUC &gt; 0.7), highlighting its potential for early screening and individualized risk assessment.</p> Conclusion <p>Our findings suggest that BaP may promote cataract development through mitochondrial dysfunction, metabolic disturbance, redox imbalance, and immune microenvironment changes mediated by core targets CCR7, CCR9, and CCL22. These results provide new insights into the pathogenesis of BaP-induced cataracts and offer potential biomarkers for early diagnosis and personalized prevention strategies.</p>

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Integrated bioinformatic analysis reveals common signaling pathways and key targets linking benzo[a]pyrene exposure to cataract progression

  • 期刊论文

  • 发表日期：

    2026年5月12日

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  • Chao HU,
  • Qun ZHANG,
  • Gongxun SUN

摘要

Background

Previous studies have shown that chemicals produced by the combustion of carbon-containing fuels, such as benzo[a]pyrene (BaP), can adversely affect chronic degenerative diseases, including cataracts. However, the molecular mechanisms underlying BaP’s role in cataract development and progression remain unclear.

Objective

This study aimed to explore the potential molecular mechanisms by which BaP contributes to the onset and progression of cataracts.

Results

By systematically analyzing databases such as ChEMBL and STITCH, we identified 57 potential targets closely related to both BaP and cataracts. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses revealed that these targets are primarily involved in mitochondrial function, cellular energy metabolism, and redox reactions. Protein–protein interaction (PPI) network analysis identified three core targets: CCR7, CCR9, and CCL22. Molecular docking demonstrated stable binding between BaP and these core proteins, suggesting their key roles in BaP-induced lens toxicity. Immune infiltration analysis indicated that the expression of these hub genes was closely associated with the abundance of various immune cell types in cataract tissues. Furthermore, ssGSEA showed significant differences in the infiltration levels of activated B cells, activated CD4 T cells, activated CD8 T cells, and regulatory T cells between groups stratified by hub gene expression. Finally, a nomogram model based on these hub genes exhibited high diagnostic accuracy for cataracts (AUC > 0.7), highlighting its potential for early screening and individualized risk assessment.

Conclusion

Our findings suggest that BaP may promote cataract development through mitochondrial dysfunction, metabolic disturbance, redox imbalance, and immune microenvironment changes mediated by core targets CCR7, CCR9, and CCL22. These results provide new insights into the pathogenesis of BaP-induced cataracts and offer potential biomarkers for early diagnosis and personalized prevention strategies.