表观遗传学
发病机制
类风湿性关节炎
免疫学
生物
后生
疾病
关节炎
机制(生物学)
电池类型
生物信息学
细胞
医学
DNA甲基化
遗传学
病理
基因表达
基因
哲学
认识论
作者
Nisha Nair,Anne Barton,Anthony G. Wilson
出处
期刊:Epigenomics
[Future Medicine]
日期:2021-04-01
卷期号:13 (7): 549-560
被引量:6
标识
DOI:10.2217/epi-2020-0380
摘要
Rheumatoid arthritis is a complex, inflammatory autoimmune disease, which is characterized by pain, swelling and joint damage driven by the altered behavior of a number of different cell types such as synovial fibroblasts macrophages and lymphocytes. The mechanism underlying pathogenesis is unclear but increasing evidence points to altered epigenetic regulation within these cell types which promotes the activated destructive behavior that underlies disease pathogenesis. This review summarizes the key epigenetic modifications in the most important cells types in rheumatoid arthritis, which are associated with disease activity. We also discuss emerging avenues of research focusing on readers of epigenetic markers which may serve to be potential therapeutic targets.
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