甲状腺相关性眼外肌病变发病机制及动物模型的研究进展  

Advances in pathogenesis and animal models of thyroid-associated extraocular myopathy

作　　者：彭玉琴 闵晓珊[1] Peng Yu-qi;Min Xiao-shan(Eye Center of Xiangya Hospital,Central South University,Changsha 410008,China)

机构地区：[1]中南大学湘雅医院眼科中心,410008

出　　处：《中国斜视与小儿眼科杂志》2023年第1期47-47,I0016,共2页Chinese Journal of Strabismus & Pediatric Ophthalmology

基　　金：湖南省自然科学基金(S2019JJMSXM2626)。

摘　　要：甲状腺相关眼病以眼眶炎症浸润、组织扩张重塑为特征。眼外肌纤维化是较复杂、且不可逆的病理学过程之一。其发病机制尚不完全清楚。眼眶成纤维细胞(Orbital fibroblasts,OFs)既是自身免疫的靶细胞,也是效应细胞。OFs表达自身抗原,包括促甲状腺激素受体(TSHR)和胰岛素样生长因子-1受体(IGF-1R)。自身抗体和炎症因子激活的OFs分泌多种趋化分子和炎症介质,在眼外肌中发挥促炎和促纤维化双向调节作用。OFs存在异质性,不同的表型转化是TAO眼外肌纤维化的重要途径。本文就甲状腺相关性眼外肌病变的发病机制及相关动物模型做一综述。Thyroid-associated ophthalmopathy is characterized by orbital inflammatory infiltration and tissue expansion and remodeling,Extraocular muscle fibrosis is one of the more complex and irreversible pathological processes.Its pathogenesis is not entirely clear.Orbital fibroblasts(OFs)are both target cells and effector cells of autoimmunity.OFs express autoantigens,including thyroid-stimulating hormone receptor(TSHR)and insulin-like growth factor-1 receptor(IGFIR).OFs activated by autoantibodies and inflammatory factors secrete a variety of chemokines and inflammatory mediators,and play a dual role of pro-inflammatory and pro-fibrotic regulation in extraocular muscles.OFs are heterogeneous,and different phenotypic transformation is an important way of extraocular muscle fibrosis in TAO.This review discusses the pathogenesis of thyroid-associated extraocular myopathy and related animal models.

关 键 词：甲状腺相关性眼病 眼眶成纤维细胞 眼外肌病理改变 限制性斜视 动物模型 

分 类 号：R771.3[医药卫生—眼科] R581[医药卫生—临床医学] R-332