ArticleJCI insight2024
Transcriptomic profiling of thyroid eye disease orbital fat demonstrates differences in adipogenicity and IGF-1R pathway.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Reduction in extraocular muscle and orbital fat volumes after teprotumumab treatment in Japanese patients with thyroid eye disease: an exploratory magnetic resonance imaging analysis from the OPTIC-J trial.Japanese journal of ophthalmology · 2026Trial
- Post Hoc MRI Analysis of Orbital Soft Tissue Volumes Pre- and Post-Teprotumumab in Patients with Chronic, Low-Activity Thyroid Eye Disease.Ophthalmology and therapy · 2026Article
- Article
- A bispecific-aptamer TSHR-CD80-1 treats thyroid eye disease by inhibiting CD8Cell communication and signaling : CCS · 2026Article
- What has changed in thyroid eye disease in the last five years (2020-2025).European thyroid journal · 2026Review
- Transcriptome analysis of orbital tissue in thyroid eye disease uncovers key pathogenic mediators.Scientific reports · 2025Article
- Unravelling the pathogenic mechanisms in Graves' orbitopathy.European thyroid journal · 2025Review
- Fibroblast PI3K/AKT signaling and extracellular matrix homeostasis: mechanisms, targets, and delivery challenges.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
8 authors.
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Abstract
Despite recent advances in the treatment of thyroid eye disease thyroid-related eye disease (TED), marked gaps remain in our understanding of the underlying molecular mechanisms, particularly concerning the insulin-like growth factor-1 receptor (IGF-1R) pathway. To dissect the pathophysiology of TED, we used single-nucleus RNA-Seq to analyze orbital fat specimens from both patients with TED and matched individuals acting as controls. The analysis demonstrated a marked increase in the proportion of fibroblasts transitioning to adipogenesis in the orbital fat of patients with TED compared with that in control patients. This was associated with diverse alterations in immune cell composition. Significant alterations in the IGF-1R signaling pathway were noted between TED specimens and those from control patients, indicating a potential pathological mechanism driven by IGF-1R signaling abnormalities. Additionally, our data showed that linsitinib, a small-molecule inhibitor of IGF-1R, effectively reduced adipogenesis in TED orbital fibroblasts in vitro, suggesting its potential utility as a therapeutic agent. Our findings reveal that, beyond immune dysfunction, abnormal IGF-1R signaling leading to enhanced adipogenesis is a crucial pathogenic mechanism in TED.
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Registered trials
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