DNA甲基化对人类风湿关节炎成纤维样滑膜细胞表观遗传调控的研究进展  

Research progress of DNA methylation on epigenetic regulation of human rheumatoid arthritis fibroblast-like synoviocytes

作　　者：苗茁 曹梅琳 周海舟[1] Miao Zhuo;Cao Meilin;Zhou Haizhou(Department of Laboratory,the First Affiliated Hospital of Harbin Medical University,Harbin 150001,China)

机构地区：[1]哈尔滨医科大学附属第一医院检验科,哈尔滨150001

出　　处：《国际免疫学杂志》2022年第5期498-502,共5页International Journal of Immunology

基　　金：国家自然科学基金(81772261)。

摘　　要：类风湿关节炎(rheumatoid arthritis,RA)是一种由免疫介导的慢性炎症性疾病,以滑膜增生和关节破坏为特征,并受遗传和环境因素影响。然而,现有证据表明,遗传多样性和环境暴露并不能解释RA的所有临床特征和异质性,而且越来越多的研究显示表观遗传调控,尤其是DNA甲基化,可在人RA成纤维样滑膜细胞(RA fibroblast-like synoviocytes,RAFLS)中促进疾病的发展,并可能参与RA的发病。文章对RA的发病机制以及RAFLS中DNA甲基化调控进行介绍,并且简要介绍了有关疾病进展及治疗的潜在生物标志物。Rheumatoid arthritis(RA)is a chronic inflammatory disease mediated by immunity.It is characterized by synovial hyperplasia and joint destruction,and is affected by genetic and environmental factors.However,existing evidence showed that the clinical characteristics and heterogeneity of RA were not only related to genetic diversity and environmental exposure.More and more studies have showed that epigenetic regulation,especially DNA methylation,can promote the development of the disease in RA fibroblast-like synoviocytes(RAFLS)and may be involved in the pathogenesis of RA.This review introduced the pathogenesis of RA and the regulation of DNA methylation in RAFLS,and briefly introduces some potential biomarkers of disease progression and treatment.

关 键 词：人类风湿关节炎成纤维样滑膜细胞 自身免疫病 DNA甲基化 表观遗传调控 

分 类 号：R593.22[医药卫生—内科学]