类风湿关节炎破骨细胞的活化机制及其预测指标

Mechanism of osteoclast activation and its predictors in rheumatoid arthritis

类风湿关节炎(rheumatoid arthritis, RA)是一种系统性、慢性、炎性的自身免疫性疾病。骨破坏在RA的发生和发展中占有重要地位,是RA致残致畸的主要原因。破骨细胞(osteoclast, OC)的异常增生与活化对RA骨侵蚀的发病进展具有重要作用。近年来,RA患者骨破坏的研究逐渐增多。本文结合国内外研究对核因子-κB受体活化因子配体(receptor activation for nuclear factor-κB ligand, RANKL)/核激活因子受体(receptor activator for nuclear factor-κB, RANK)/骨保护素(orthopantomography, OPG)信号通路、Wnt信号通路、抗瓜氨酸蛋白抗体(anti-citrulline protein antibody, ACPA)、基质金属蛋白酶(matrixmetalloproteinases,MMPs)、14-3-3η蛋白、基质细胞衍生因子-1(stromalcellderivedfactor-1,SDF-1)、小泛素样修饰物蛋白(smallubiquitin-likemodifierprotein,SUMO)、分泌型卷曲相关蛋白(secreted frizzled-related protein, SFRP)、骨转换标志物等作一阐述,旨在为RA早期骨破坏诊断提供相关依据。

Rheumatoid arthritis(RA) is a systemic, chronic and inflammatory autoimmune disease. Bone destruction plays an important role in the occurrence and development of RA. Abnormal proliferation and activation of osteoclasts(OC) play an important role in the development of RA bone erosion. In recent years, studies on osteoclasts and bone destruction in RA patients have gradually increased. We briefly described the research of receptor activation for nuclear factor-κB ligand/receptor activator for nuclear factor-κB/orthopantomography(RANKL/RANK/OPG) signaling pathway, Wnt signaling pathways, cytokines, anti-citrulline protein antibody(ACPA), matrix metalloproteinases(MMPs), the 14-3-3η protein and stromal cell derived factor-1(SDF-1), small ubiquitin-like modifier protein(SUMO) and secreted frizzled-related protein(SFRP), bone conversion markers and so on, to provide evidences for early RA bone damage diagnosis.