Dept of Internal Medicine and Rheumatology, Justus-Liebig-University Gießen, Kerckhoff-Klinik, Benekestr. 2-8, D-61231 Bad Nauheim, Germany.
Trends Mol Med. 2010 Oct;16(10):458-68. doi: 10.1016/j.molmed.2010.07.004. Epub 2010 Aug 24.
Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by synovial hyperplasia and progressive joint destruction. Rheumatoid arthritis synovial fibroblasts (RASFs) are leading cells in joint erosion and contribute actively to inflammation. RASFs show an activated phenotype that is independent of the inflammatory environment and requires the combination of several factors. Although new aspects regarding RASF activation via matrix degradation products, epigenetic modifications, inflammatory factors, Toll-like receptor (TLR) activation and others have recently been uncovered, the primary pathophysiological processes in early arthritis leading to permanent activation are mostly unknown. Here, we review new findings regarding RASF activation and their altered behavior that contribute to matrix destruction and inflammation as well as their potential to spread RA.
类风湿关节炎（RA）是一种慢性炎症性疾病，其特征为滑膜增生和进行性关节破坏。类风湿关节炎滑膜成纤维细胞（RASFs）是关节侵蚀的主要细胞，并积极参与炎症反应。RASFs 表现出一种激活表型，这种表型不依赖于炎症环境，需要几种因素的结合。尽管最近发现了通过基质降解产物、表观遗传修饰、炎症因子、Toll 样受体（TLR）激活等途径导致 RASF 激活的新方面，但导致早期关节炎永久性激活的主要病理生理过程在很大程度上尚不清楚。在这里，我们综述了关于 RASF 激活及其改变行为的新发现，这些发现导致了基质破坏和炎症，并可能导致 RA 的传播。
