Abstract
Background
Thyroid eye disease (TED) is a vision-threatening autoimmune disorder, and the molecular mechanisms underlying thyroid eye disease (TED), particularly those independent of typical Graves’ Disease (GD) signals, remain unclear.
Objective
This study aimed to identify upregulated differentially expressed genes (DEGs) and hub genes in TED after the indirect exclusion of GD-associated signals, and explore their potential biological functions in an exploratory context.
Methods
We collected datasets from the Gene Expression Omnibus and analyzed DEGs using the “limma” package. Enrichment analyses were conducted to investigate the biological processes and pathways. Upregulated hub DEGs in TED after the indirect exclusion of GD-associated signals were identified through various algorithms. A nomogram model was developed based on diagnostic biomarkers, and its reliability was evaluated. Immune infiltration analyses were also performed.
Results
Our results identified upregulated DEGs and hub genes in TED after the indirect exclusion of GD-associated signals, which were enriched in specific biological processes and pathways. The nomogram model showed good calibration and diagnostic value.
Conclusion
These findings provide exploratory insights into the molecular mechanisms of TED. Further validation in larger, well-characterized cohorts is essential to confirm these results before any clinical application.
Keywords
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