ArticleThe Journal of clinical endocrinology and metabolism2025
A Preclinical State of Graves' Ophthalmopathy Characterized by Hypoxia of T-cells Identified via Multiomics Analysis.
Article in The Journal of clinical endocrinology and metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Integrative transcriptomic profiling and machine learning reveal hypoxia-associated molecular signatures for precision diagnosis in thyroid eye disease.Human genomics · 2025Article
- Multidimensional predictive model for assessing clinical activity in thyroid eye disease.Frontiers in medicine · 2025Article
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Authors and funding
15 authors.
Funding
Abstract
contextA preclinical state of Graves' ophthalmopathy (pre-GO) exists during the progression from Graves' hyperthyroidism (GH) to GO.
objectiveTo distinguish the pre-GO state and identify key pathways of T-cell immunity.
methodsTwenty-four GH (without ophthalmopathy within 6-month follow-up), 10 pre-GO (ophthalmopathy occurred within 6-month follow-up), and 21 GO patients were enrolled, and the transcription and DNA methylation profiles of peripheral blood mononuclear cells were generated. The differentially expressed genes (DEGs), differentially methylated CpG sites (DMCs), and differentially methylated genes (DMGs) were identified. Cluster analysis, functional analysis, and data integration analysis using latent components (DIABLO) were performed to distinguish pre-GO and identify key pathways. Flow cytometry was performed for in vitro verification.
resultsIn total, 731, 1214, and 372 DEGs and 1583, 277, and 555 DMCs were detected via pairwise comparisons of GH vs GO, pre-GO vs GO, and GH vs pre-GO, respectively. DIABLO accurately discriminated the pre-GO state via 17 DMC and 11 DEG features ( receiver operating characteristic = 0.9975 and 0.9407, respectively). The functional analysis revealed that the DMGs and DEGs were enriched in T-cell differentiation pathways and related cytokine pathways, respectively. Further cluster analysis revealed a cluster of pre-GO-specific DEGs enriched in the hypoxia pathway. Flow cytometry confirmed that hypoxia promoted Th1, Th17, and antigen-specific CD4+ cytotoxic T-cell differentiation.
conclusionThe pre-GO state was identified from GH and GO and characterized by upregulation of the hypoxia pathway that may promote effector CD4+ T-cells differentiation. These findings provide new insight into the pathogenesis and prevention of GO.
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