ArticleActa endocrinologica (Bucharest, Romania : 2005)
BIOINFORMATIC ANALYSIS IDENTIFIES POTENTIALLY KEY DIFFERENTIALLY EXPRESSED GENES AND PATHWAYS IN ORBITAL ADIPOSE TISSUES OF PATIENTS WITH THYROID EYE DISEASE.
Article in Acta endocrinologica (Bucharest, Romania : 2005). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 7 citations in OpenAlex.
- Maraviroc attenuates orbital remodeling, inflammation, and lipid dysregulation in a murine model of thyroid eye disease associated with Graves' disease.Frontiers in endocrinology · 2026Article
- Macrophage plasticity in thyroid eye disease: dual effects of inflammation and fibrosis.Frontiers in immunology · 2026Review
- Hub genes and key pathways of Graves' disease: bioinformatics analysis and validation.Hormones (Athens, Greece) · 2025Article
- Review
- Construction of the coexpression network involved in the pathogenesis of thyroid eye disease via bioinformatics analysis.Human genomics · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
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Abstract
contextThyroid eye disease (TED), an orbital inflammatory status, generally occurred in Graves' disease.
objectiveThis study aimed to acquire further insight into molecular mechanisms of TED, especially several key involved genes and pathways.
designThe microarray dataset GSE58331 including expression data for orbital adipose tissue samples, isolated from TED patients and normal controls, was downloaded from a publicly accessible Gene Expression Omnibus database. Differentially expressed genes (DEGs) were identified from 23 adipose tissues of TED patients SUBJECTS AND
methodsA protein-protein interaction network of DEGs was constructed by using Search Tool for the Retrieval of Interacting Genes and Cytoscape 3.6.0. Several hub genes/proteins were extracted from the protein-protein interaction network based on connectivity degree. Furthermore, we used the iRegulon plugin of Cytoscape3.6.0 to predict the transcription factors (TFs).
resultsA total of 678 DEGs (538 up- and 140 down-regulated genes) were identified in TED patients. Proopiomelanocortin (POMC), interleukin 2 (IL-2), G protein subunit gamma 3 (GNG3), CXC motif chemokine receptor 4 (CXCR4), toll like receptor 4 (TLR4), colony stimulating factor 1 receptor (CSF1R), lysophosphatidic acid receptor 3 (LPAR3), CXC motif chemokine ligand-8 (CXCL8), etc., were considered as the hub genes among the DEGs. There were 6 TFs predicted to be differentially expressed in regulating the DEGs related to TED. A total of 71 DEGs had been reported to be associated with TED in the Comparative Toxicogenomics Database.
conclusionsThrough this analysis, we have identified plenty of potential biomarkers and pathways which may have an important role in the pathogenesis of TED. However, these findings require verification by more detailed future experimental studies.
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