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<p>Fuchs’ Endothelial Corneal Dystrophy (FECD) is a slowly advancing, non-inflammatory eye condition due to a gradual increase in the thickness of the Descemet’s membrane and the gradual decline in the corneal endothelial cell population. It can occur sporadically or be inherited in an autosomal dominant manner, leading to impaired vision over time. Corneal transplantation is currently the only treatment for FECD. This study aims to identify potential biomarkers, pathways, and therapeutic targets to treat FECD. The dataset GSE171830 was retrieved from Gene Expression Omnibus (GEO) database for the purpose of investigating and identifying potential therapeutic targets for FECD. Using the GEO2R tool, 2654 differentially expressed genes (DEGs) were identified, with 1763 upregulated and 881 downregulated genes, for annotating FECD pathogenesis pathways. We conducted gene enrichment analysis with the aim of identifying the pathways associated with FECD disease. Selected DEGs functional annotations show the involvement of several FECD-related biological processes and pathways. Our findings unravel potential biomarkers, including <i>HLA-DRA</i>, <i>CSF1R</i>, <i>TNFRSF11B</i>, <i>COL4A1</i>, etc., through GO, KEGG analysis, and Protein–Protein Interaction (PPI). Among them, we considered two targets, viz. CSF1R, TNFRSF11B due to their small molecule binding pockets. Further, virtual screening was performed against 61 FDA-approved eye care drugs, and we identified the top five drugs for each target, and the results are discussed in detail. The findings from this study could offer novel insights into the molecular mechanism of FECD, and the identified drugs could have a significant impact on the treatment and prevention of FECD.</p> Graphical abstract <p></p>

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Biomarker driven drug repurposing for Fuchs’ endothelial corneal dystrophy (FECD): a computational study

  • 期刊论文

  • 发表日期：

    2025年12月9日

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  • Sarangthem Dinamani Singh,
  • Gayatri Gogoi,
  • Selvaraman Nagamani,
  • Pankaj Bharali

摘要

Fuchs’ Endothelial Corneal Dystrophy (FECD) is a slowly advancing, non-inflammatory eye condition due to a gradual increase in the thickness of the Descemet’s membrane and the gradual decline in the corneal endothelial cell population. It can occur sporadically or be inherited in an autosomal dominant manner, leading to impaired vision over time. Corneal transplantation is currently the only treatment for FECD. This study aims to identify potential biomarkers, pathways, and therapeutic targets to treat FECD. The dataset GSE171830 was retrieved from Gene Expression Omnibus (GEO) database for the purpose of investigating and identifying potential therapeutic targets for FECD. Using the GEO2R tool, 2654 differentially expressed genes (DEGs) were identified, with 1763 upregulated and 881 downregulated genes, for annotating FECD pathogenesis pathways. We conducted gene enrichment analysis with the aim of identifying the pathways associated with FECD disease. Selected DEGs functional annotations show the involvement of several FECD-related biological processes and pathways. Our findings unravel potential biomarkers, including HLA-DRA, CSF1R, TNFRSF11B, COL4A1, etc., through GO, KEGG analysis, and Protein–Protein Interaction (PPI). Among them, we considered two targets, viz. CSF1R, TNFRSF11B due to their small molecule binding pockets. Further, virtual screening was performed against 61 FDA-approved eye care drugs, and we identified the top five drugs for each target, and the results are discussed in detail. The findings from this study could offer novel insights into the molecular mechanism of FECD, and the identified drugs could have a significant impact on the treatment and prevention of FECD.

Graphical abstract