Ji Minjeong, Ryu Hee Jung, Hong Jeong Hee
Department of Physiology, College of Medicine, Gachon University, Lee Gil Ya Cancer and Diabetes Institute, Incheon, South Korea.
Department of Rheumatology, Gachon University Gil Medical Center, Incheon, South Korea.
Bone Joint Res. 2021 Apr;10(4):285-297. doi: 10.1302/2046-3758.104.BJR-2020-0331.R1.
Rheumatoid arthritis (RA) is an autoimmune disease characterized by symmetrical and chronic polyarthritis. Fibroblast-like synoviocytes are mainly involved in joint inflammation and cartilage and bone destruction by inflammatory cytokines and matrix-degrading enzymes in RA. Approaches that induce various cellular growth alterations of synoviocytes are considered as potential strategies for treating RA. However, since synoviocytes play a critical role in RA, the mechanism and hyperplastic modulation of synoviocytes and their motility need to be addressed. In this review, we focus on the alteration of synoviocyte signalling and cell fate provided by signalling proteins, various antioxidant molecules, enzymes, compounds, clinical candidates, to understand the pathology of the synoviocytes, and finally to achieve developed therapeutic strategies of RA. Cite this article: 2021;10(4):285-297.
类风湿性关节炎(RA)是一种以对称性慢性多关节炎为特征的自身免疫性疾病。在类风湿性关节炎中,成纤维样滑膜细胞主要通过炎性细胞因子和基质降解酶参与关节炎症以及软骨和骨破坏。诱导滑膜细胞发生各种细胞生长改变的方法被视为治疗类风湿性关节炎的潜在策略。然而,由于滑膜细胞在类风湿性关节炎中起关键作用,因此滑膜细胞的机制、增生调节及其运动性仍需深入研究。在本综述中,我们重点关注信号蛋白、各种抗氧化分子、酶、化合物、临床候选药物所引起的滑膜细胞信号传导和细胞命运的改变,以了解滑膜细胞的病理学,最终实现针对类风湿性关节炎的有效治疗策略。引用本文:2021;10(4):285 - 297。