ReviewInternational ophthalmology2025
Molecular pathway and mechanism responsible for the progress of thyroid-associated orbitopathy.
Review in International ophthalmology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed.
- Metabolic reprogramming of Th17/Treg imbalance in autoimmune thyroid diseases.Cell communication and signaling : CCS · 2026Review
- Molecular imaging of fibroblast activation in systemic sclerosis using [European journal of nuclear medicine and molecular imaging · 2026Article
- Puerarin suppress adipogenesis and inflammation on orbital fibroblasts from patients with thyroid eye disease.Journal of endocrinological investigation · 2026Article
- Retinal Microvascular and Orbital Structural Alterations in Thyroid Eye Disease.Journal of clinical medicine · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeOur study aims to summarize the current knowledge concerning the molecular pathway and mechanism responsible for the progress of orbitopathy in the thyroid.
methodA thorough investigation of the literature was conducted using Scopus, Elsevier, PubMed, ScienceDirect, and Web of Science databases, covering studies published between 2000 and 2024. The inclusion criteria focused on clinical trials, preclinical research, and ethnopharmacological studies that investigated the effects of traditional medicines on "orbitopathy in thyroid," "molecular pathway," "mechanism," "Medicinal Plants," "Mechanism of Action," and "Active Constituents." Studies were excluded if they lacked specific data on orbitopathy in thyroid, focused solely on orbitopathy in thyroid, or had inconclusive methodologies.
resultsOur findings indicate that TSHR autoantibodies drive orbital fibroblast activation, leading to inflammation, adipogenesis, and glycosaminoglycan accumulation. Elevated IL-17 and TNF-α levels contribute to immune dysregulation, while IGF-1R signaling enhances fibroblast proliferation and cytokine release. Biomarker analysis suggests that miR-146a, miR-155, and HLA-DR3 polymorphisms may serve as potential indicators for disease severity and progression.
conclusionEarly diagnostic markers and targeted therapies, including offer promising avenues for improved TAO management. A multidisciplinary, personalized approach integrating biomarker-driven treatment decisions may help optimize patient outcomes.
Indexed as
Identifiers
40381066What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.