Rheumatoid arthritis progression mediated by activated synovial fibroblasts

被引：364

作者：

Neumann, Elena ^{[1
]}

Lefevre, Stephanie ^{[1
]}

Zimmermann, Birgit ^{[1
]}

Gay, Steffen ^{[2
]}

Mueller-Ladner, Ulf ^{[1
]}

机构：

[1] Univ Giessen, Dept Internal Med & Rheumatol, Kerckhoff Klin, D-61231 Bad Nauheim, Germany

[2] Univ Zurich Hosp, Dept Rheumatol, CH-8091 Zurich, Switzerland

来源：

TRENDS IN MOLECULAR MEDICINE | 2010年 / 16卷 / 10期

关键词：

NECROSIS-FACTOR-ALPHA; TOLL-LIKE RECEPTORS; PROSTAGLANDIN E-2 PRODUCTION; ENDOTHELIAL GROWTH-FACTOR; NF-KAPPA-B; INDUCED APOPTOSIS; MATRIX-METALLOPROTEINASE; THERAPEUTIC IMPLICATIONS; INFLAMMATORY ARTHRITIS; FACTOR-BETA;

D O I：

10.1016/j.molmed.2010.07.004

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：458 / 468

页数：11

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