Liu Shan-Chi, Law Yat-Yin, Wu Yu-Ying, Huang Yuan-Li, Tsai Chun-Hao, Chen Wei-Cheng, Tang Chih-Hsin
Institute of Biomedical Sciences, Mackay Medical College, New Taipei City 23245, Taiwan, R.O.C.
School of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan, R.O.C.
Mol Med Rep. 2025 May;31(5). doi: 10.3892/mmr.2025.13489. Epub 2025 Mar 14.
Osteoarthritis (OA) is a long‑term, degenerative joint disease that presents significant clinical challenges and imposes considerable financial burdens. Fibrosis is closely intertwined with the pathogenesis of various degenerative diseases, including OA. Using data from the GDS5401 dataset, the present study determined that expression levels of the fibrosis factor connective tissue growth factor (CTGF) were significantly higher in OA patients than in normal individuals. The present study also identified CTGF elevated expression levels in both OA patients compared with healthy controls and in rats with anterior cruciate ligament transection‑induced OA versus controls. Stimulating OA synovial fibroblasts (OASFs) with CTGF was shown to promote vascular cell adhesion molecule‑1 (VCAM‑1) production, thereby facilitating monocyte adhesion to OASFs. Analysis of a large dataset revealed that monocytes are the only mononuclear cells with significantly elevated levels in OA patients. It also appeared that CTGF‑induced VCAM‑1 production and monocyte adhesion were mediated via the focal adhesion kinase and JNK pathways. These findings suggest that CTGF contributes to OA progression by enhancing monocyte adhesion to the synovial membrane.
骨关节炎（OA）是一种长期的退行性关节疾病，带来了重大的临床挑战并造成了相当大的经济负担。纤维化与包括OA在内的各种退行性疾病的发病机制密切相关。本研究利用GDS5401数据集的数据确定，纤维化因子结缔组织生长因子（CTGF）在OA患者中的表达水平显著高于正常个体。本研究还发现，与健康对照相比，OA患者以及前交叉韧带横断诱导的OA大鼠与对照相比，CTGF的表达水平均升高。用CTGF刺激OA滑膜成纤维细胞（OASF）可促进血管细胞黏附分子-1（VCAM-1）的产生，从而促进单核细胞黏附于OASF。对一个大型数据集的分析显示，单核细胞是OA患者中唯一水平显著升高的单核细胞。此外，CTGF诱导的VCAM-1产生和单核细胞黏附似乎是通过黏着斑激酶和JNK途径介导的。这些发现表明，CTGF通过增强单核细胞对滑膜的黏附作用促进OA的进展。
