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February 5, 2026Medicine0 citationsOpen Access

Ferroptosis in glaucoma: Identification of key genes NR1D2 and AKR1C3 based on transcriptome bioinformatics analysis

WHWenwen HaoZHZhu HuangFXFang Xu

Key Points

  • This research aims to identify and evaluate genes related to ferroptosis in glaucoma using transcriptome data analysis.
  • Analyzed GEO datasets GSE9944 and GSE2378
  • Employed least absolute shrinkage and selection operator (LASSO)
  • Utilized support vector machine-recursive feature elimination methods
  • Applied bioinformatics tools for diagnostic assessment
  • Conducted drug sensitivity and competitive endogenous RNA network analyses
  • Identified NR1D2 and AKR1C3 as key ferroptosis-related genes
  • Both genes showed high diagnostic potential for glaucoma
  • Involved in redox reactions and immune responses
  • Confirmed as potential therapeutic targets and biomarkers

Abstract

Glaucoma, a leading cause of blindness, involves retinal ganglion cell death linked to ferroptosis, an iron-dependent form of cell death. This study analyzed GEO datasets (GSE9944 and GSE2378) to identify ferroptosis-related genes in glaucoma. Least absolute shrinkage and selection operator and support vector machine-recursive feature elimination methods were used to select key genes, and bioinformatics tools were applied to assess their diagnostic potential and biological significance. NR1D2 and AKR1C3 were identified as key ferroptosis-related genes with high diagnostic potential. These genes are involved in redox reactions, cellular processes, and immune responses. Drug sensitivity and competitive endogenous RNA network analyses further confirmed their value as potential diagnostic biomarkers and therapeutic targets. NR1D2 and AKR1C3 are promising biomarkers for diagnosing glaucoma and serve as potential therapeutic targets, offering new insights into its pathogenesis and treatment strategies.

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Cite This Study

Hao et al. (2026) studied this question.

synapsesocial.com/papers/69843398f1d9ada3c1fb0dcchttps://doi.org/10.1097/md.0000000000047370
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