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.

PubMed
Abstract

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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