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Abstract：
Osteoarthritis (OA) is the most common form of arthritis, characterized by osteophyte formation, cartilage degradation, and structural and cellular alterations of the synovial membrane. Activated fibroblast-like synoviocytes (FLS) of the synovial membrane have been identified as key drivers, secreting humoral mediators that maintain inflammatory processes, proteases that cause cartilage and bone destruction, and factors that drive fibrotic processes. In normal tissue repair, fibrotic processes are terminated after the damage has been repaired. In fibrosis, tissue remodeling and wound healing are exaggerated and prolonged. Various stressors, including aging, joint instability, and inflammation, lead to structural damage of the joint and micro lesions within the synovial tissue. One result is the reduced production of synovial fluid (lubricants), which reduces the lubricity of the cartilage areas, leading to cartilage damage. In the synovial tissue, a wound-healing cascade is initiated by activating macrophages, Th2 cells, and FLS. The latter can be divided into two major populations. The destructive thymocyte differentiation antigen (THY)1─ phenotype is restricted to the synovial lining layer. In contrast, the THY1+ phenotype of the sublining layer is classified as an invasive one with immune effector function driving synovitis. The exact mechanisms involved in the transition of fibroblasts into a myofibroblast-like phenotype that drives fibrosis remain unclear. The review provides an overview of the phenotypes and spatial distribution of FLS in the synovial membrane of OA, describes the mechanisms of fibroblast into myofibroblast activation, and the metabolic alterations of myofibroblast-like cells.
摘要：
骨关节炎（OA）是最常见的关节炎，以骨赘形成为特征，软骨退化，以及滑膜的结构和细胞改变。滑膜的成纤维细胞样滑膜细胞（FLS）已被确定为关键驱动因素，分泌维持炎症过程的体液介质，导致软骨和骨骼破坏的蛋白酶，和驱动纤维化过程的因素。在正常组织修复中，修复损伤后，纤维化过程终止。在纤维化中，组织重塑和伤口愈合被夸大和延长。各种压力源，包括衰老，关节不稳定性，和炎症，导致关节结构损伤和滑膜组织内的微病变。一个结果是滑液（润滑剂）的产生减少，这降低了软骨区域的润滑性，导致软骨损伤.在滑膜组织中，伤口愈合级联是通过激活巨噬细胞启动的，Th2细胞，和FLS。后者可分为两个主要群体。破坏性胸腺细胞分化抗原（THY）1-表型仅限于滑膜衬里层。相比之下,亚衬层的THY1+表型被归类为具有免疫效应子功能驱动滑膜炎的侵入性表型。涉及成纤维细胞转变为驱动纤维化的肌成纤维细胞样表型的确切机制仍不清楚。本文综述了OA滑膜中FLS的表型和空间分布，描述了成纤维细胞激活成肌成纤维细胞的机制，和肌成纤维细胞样细胞的代谢改变。
