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核因子κB受体活化因子配体:类风湿关节炎骨破坏的治疗靶点。

RANKL: A therapeutic target for bone destruction in rheumatoid arthritis.

作者信息

Tanaka Sakae, Tanaka Yoshiya, Ishiguro Naoki, Yamanaka Hisashi, Takeuchi Tsutomu

机构信息

a Department of Orthopaedic Surgery, Faculty of Medicine , The University of Tokyo , Tokyo , Japan.

b First Department of Internal Medicine , University of Occupational and Environmental Health , Fukuoka , Japan.

出版信息

Mod Rheumatol. 2018 Jan;28(1):9-16. doi: 10.1080/14397595.2017.1369491. Epub 2017 Sep 18.

Abstract

Rheumatoid arthritis (RA) is a chronic inflammatory disorder characterized by progressive joint destruction. Recent studies have indicated the critical involvement of osteoclasts in bone destruction in RA. The osteoclast differentiation factor receptor activator of NF-κB ligand (RANKL), which belongs to the tumor necrosis factor superfamily, plays a critical role in osteoclast differentiation and bone destruction in RA. Denosumab, an antibody against human RANKL, efficiently suppressed the progression of bone erosion in RA patients in randomized controlled studies, and is considered as a putative therapeutic option for preventing bone destruction in RA.

摘要

类风湿性关节炎(RA)是一种以进行性关节破坏为特征的慢性炎症性疾病。最近的研究表明破骨细胞在RA的骨破坏中起关键作用。属于肿瘤坏死因子超家族的破骨细胞分化因子核因子κB受体活化因子配体(RANKL)在RA的破骨细胞分化和骨破坏中起关键作用。地诺单抗是一种抗人RANKL的抗体,在随机对照研究中能有效抑制RA患者骨侵蚀的进展,被认为是预防RA骨破坏的一种潜在治疗选择。

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