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RANKL 作为类风湿关节炎的治疗靶点。

RANKL as a therapeutic target of rheumatoid arthritis.

机构信息

Department of Orthopaedic Surgery, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.

First Department of Internal Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu, Fukuoka, 807-8555, Japan.

出版信息

J Bone Miner Metab. 2021 Jan;39(1):106-112. doi: 10.1007/s00774-020-01159-1. Epub 2020 Oct 18.

Abstract

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.

摘要

类风湿关节炎(RA)是一种以进行性关节破坏为特征的炎症性疾病。最近的研究表明,破骨细胞是 RA 中骨破坏的原因。核因子κB 受体激活剂配体(RANKL)是一种破骨细胞分化因子,属于肿瘤坏死因子超家族,在破骨细胞分化中起关键作用。RA 患者的滑膜组织中 RANKL 表达水平升高,参与破骨细胞的发育和骨破坏。在一项随机对照研究中,针对人 RANKL 的特异性抗体地舒单抗有效地抑制了 RA 患者的骨破坏进展,被认为是 RA 的一种潜在治疗选择。

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