Protective Role of Optineurin Against Joint Destruction in Rheumatoid Arthritis Synovial Fibroblasts
Protective Role of Optineurin Against Joint Destruction in Rheumatoid Arthritis Synovial Fibroblasts
复制标题
DOI：
10.1002/art.41290
复制
发表时间：
2020-04
影响因子：
13.3
通讯作者：
Wen Shi Lee;M. Kato;E. Sugawara;M. Kono;Yuki Kudo;M. Kono;Y. Fujieda;T. Bohgaki;O. Amengual;K. Oku;S. Yasuda;T. Onodera;N. Iwasaki;T. Atsumi
中科院分区：
文献类型：
--
作者：
Wen Shi Lee;M. Kato;E. Sugawara;M. Kono;Yuki Kudo;M. Kono;Y. Fujieda;T. Bohgaki;O. Amengual;K. Oku;S. Yasuda;T. Onodera;N. Iwasaki;T. Atsumi
Optineurin(OPTN)是一种自噬适配器/受体，是破骨细胞分化的内在负调控因子。由类风湿关节炎滑膜成纤维细胞(RASF)表达的RANKL是RA患者骨侵蚀的主要原因。本研究的目的是探讨OPTN在RA关节破坏发病机制中的作用。
Optineurin (OPTN) is an autophagy adaptor/receptor that acts as an intrinsic negative regulator of osteoclast differentiation. RANKL expressed by rheumatoid arthritis synovial fibroblasts (RASFs) is primarily responsible for the development of bone erosions in patients with RA. The aim of the present study was to explore the role of OPTN in the pathogenesis of joint destruction in RA.