ArticleInternational journal of ophthalmology2026
Carnosic acid's mechanism in alleviating POAG-induced optic nerve injury
Article in International journal of ophthalmology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
aimTo explore the mechanism of carnosic acid (CA) in treating primary open angle glaucoma (POAG)-induced optic nerve injury using network pharmacology and bioinformatics analyses.
methodsCA targets were predicted using SwissTargetPrediction and TARGET PREDICTION databases, while glaucoma-related targets were identified
resultsA total of 306 DEGs, 84 CA targets, and 15 715 glaucoma targets were identified. FABP3 was identified as the key target, which was significantly upregulated in POAG samples in both validation datasets (GSE13534 and GSE2387) and confirmed by qRT-PCR and WB assays. Molecular docking revealed a strong binding affinity between FABP3 and CA (docking score: -9.79 kcal/mol), which was validated by Co-IP. Functional enrichment analysis showed FABP3 was associated with mitochondrial function and immune-related pathways. Correlation analysis indicated FABP3 had a significant negative correlation with activated dendritic cells (aDCs).
conclusionOur study suggests that CA may treat POAG by targeting FABP3, potentially by mitigating oxidative stress and modulating immune responses. This provides a pharmacological foundation and identifies FABP3 as a potential therapeutic target for POAG treatment.
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