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Updated: Jul 8, 2026

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
Published on: April 17, 2013
Molecular pathway and mechanism responsible for the progress of thyroid-associated orbitopathy
Jyotsana Dwivedi1, Shubhi Kaushal2, Poonam Arora3
1PSIT- Pranveer Singh Institute of Technology (Pharmacy), Kanpur, India. dwivedijyotsana2010@gmail.com.
Purpose:
Our study aims to summarize the current knowledge concerning the molecular pathway and mechanism responsible for the progress of orbitopathy in the thyroid.
Method:
A 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.
Results:
Our 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.
Conclusion:
Early 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.
Insights
Thyroid orbitopathy involves TSHR autoantibodies activating orbital fibroblasts, causing inflammation and tissue changes. Biomarkers like miR-146a may predict disease progression, aiding targeted therapy development.
Area of Science:
- Endocrinology
- Immunology
- Molecular Biology
Background:
- Thyroid orbitopathy (TO) is an autoimmune condition affecting the eye socket.
- Understanding its molecular mechanisms is crucial for effective treatment.
Purpose of the Study:
- To synthesize current knowledge on the molecular pathways and mechanisms driving thyroid orbitopathy progression.
- To identify potential diagnostic markers and therapeutic targets.
Main Methods:
- Comprehensive literature review of studies from 2000-2024.
- Inclusion of clinical trials, preclinical research, and ethnopharmacological studies.
- Focused search on keywords related to thyroid orbitopathy, molecular pathways, and traditional medicines.
Main Results:
- TSHR autoantibodies activate orbital fibroblasts, leading to inflammation, adipogenesis, and glycosaminoglycan accumulation.
- Elevated IL-17 and TNF-α indicate immune dysregulation; IGF-1R signaling promotes fibroblast activity.
- miR-146a, miR-155, and HLA-DR3 polymorphisms show potential as biomarkers for disease severity.
Conclusions:
- Early diagnostic markers and targeted therapies offer improved management for thyroid-associated orbitopathy (TAO).
- A personalized, biomarker-driven approach is recommended for optimizing patient outcomes.
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