Molecular pathway and mechanism responsible for the progress of thyroid-associated orbitopathy.

IF 1.4 4区医学 Q3 OPHTHALMOLOGY

International Ophthalmology Pub Date : 2025-05-17 DOI:10.1007/s10792-025-03564-9

Jyotsana Dwivedi, Shubhi Kaushal, Poonam Arora, Pranay Wal, Ankita Wal, Amin Gasmi

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引用次数: 0

Abstract

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.

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甲状腺相关性眼病进展的分子途径和机制。

目的：本研究旨在总结目前关于甲状腺眼病进展的分子途径和机制的研究进展。方法：利用Scopus、Elsevier、PubMed、ScienceDirect和Web of Science数据库对2000年至2024年间发表的文献进行全面调查。纳入标准侧重于临床试验、临床前研究和民族药理学研究，这些研究调查了传统药物对“甲状腺眼病”、“分子途径”、“机制”、“药用植物”、“作用机制”和“活性成分”的影响。如果缺乏甲状腺眼病的具体数据，仅关注甲状腺眼病，或方法不确定，则排除研究。结果：我们的研究结果表明，TSHR自身抗体驱动眼眶成纤维细胞活化，导致炎症、脂肪生成和糖胺聚糖积累。IL-17和TNF-α水平升高有助于免疫失调，而IGF-1R信号传导促进成纤维细胞增殖和细胞因子释放。生物标志物分析表明，miR-146a、miR-155和HLA-DR3多态性可能是疾病严重程度和进展的潜在指标。结论：早期诊断标志物和靶向治疗为改善TAO的管理提供了有希望的途径。多学科，个性化的方法整合生物标志物驱动的治疗决策可能有助于优化患者的结果。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

International Ophthalmology OPHTHALMOLOGY-

CiteScore

3.20

自引率

0.00%

发文量

451

期刊介绍： International Ophthalmology provides the clinician with articles on all the relevant subspecialties of ophthalmology, with a broad international scope. The emphasis is on presentation of the latest clinical research in the field. In addition, the journal includes regular sections devoted to new developments in technologies, products, and techniques.