Yuan Feng-Lai, Li Xia, Xu Rui-Sheng, Jiang Dong-Lin, Zhou Xiao-Gang
Department of Orthopaedics and Central Laboratory, The Third Hospital Affiliated to Nantong University, Wuxi, 214041, Jiangsu, China.
Cell Biochem Biophys. 2014 Sep;70(1):77-82. doi: 10.1007/s12013-014-9913-8.
Rheumatoid arthritis (RA) is an immune-mediated disease of unknown cause that primarily affects the joints and ultimately leads to joint destruction. In recent years, the potential role of DNA methylation in the development of RA is raising great expectations among clinicians and researchers. DNA methylation influences diverse aspects of the disease and regulates epigenetic silencing of genes and behavior of several cell types, especially fibroblast-like synoviocytes (FLS), the most resident cells in joints. The activation of FLS is generally regarded as a key process in the development of RA that actively results in the promotion of ongoing inflammation and joint damage. It has also been shown that aberrant DNA methylation occurs in the pathogenesis of RA and contributes to the development of the disease. Recently, there has been an impressive increase in studies involving DNA methylation in RA. In this paper, we consider the role of DNA methylation in the development of RA.
类风湿性关节炎（RA）是一种病因不明的免疫介导疾病，主要影响关节并最终导致关节破坏。近年来，DNA甲基化在RA发病过程中的潜在作用引起了临床医生和研究人员的高度期望。DNA甲基化影响疾病的多个方面，并调节基因的表观遗传沉默以及几种细胞类型的行为，尤其是成纤维样滑膜细胞（FLS），即关节中最主要的驻留细胞。FLS的激活通常被认为是RA发病过程中的关键环节，它会积极促进炎症持续发展和关节损伤。研究还表明，异常DNA甲基化发生在RA的发病机制中，并促进疾病的发展。最近，涉及RA中DNA甲基化的研究显著增加。在本文中，我们探讨DNA甲基化在RA发病过程中的作用。
