RANKL as a therapeutic target of rheumatoid arthritis

被引:33
|
作者
Tanaka, Sakae [1 ]
Tanaka, Yoshiya [2 ]
机构
[1] Univ Tokyo, Dept Orthopaed Surg, Fac Med, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1130033, Japan
[2] Univ Occupat & Environm Hlth, Dept Internal Med 1, Yahatanishi Ku, 1-1 Iseigaoka, Kitakyushu, Fukuoka 8078555, Japan
关键词
Rheumatoid arthritis; Osteoclast; RANKL; Denosumab; MODIFYING ANTIRHEUMATIC DRUGS; BONE-MINERAL DENSITY; ZOLEDRONIC ACID; DOUBLE-BLIND; DIFFERENTIATION FACTOR; EULAR RECOMMENDATIONS; SYNOVIAL FIBROBLASTS; STRUCTURAL DAMAGE; JAPANESE PATIENTS; TNF-ALPHA;
D O I
10.1007/s00774-020-01159-1
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Rheumatoid arthritis (RA) is an inflammatory disorder characterized by progressive joint destruction. Recent studies have demonstrated that osteoclasts are responsible for bone destruction in RA. Receptor activator of nuclear factor kappa B ligand (RANKL), an osteoclast differentiation factor, belongs to the tumor necrosis factor superfamily and plays a critical role in osteoclast differentiation. RANKL is highly expressed in the synovial tissues in patients with RA and is involved in osteoclast development and thus bone destruction in RA. Denosumab, a specific antibody to human RANKL, efficiently suppressed the progression of bone destruction in patients with RA in a randomized controlled study and is considered a putative therapeutic option for RA.
引用
收藏
页码:106 / 112
页数:7
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