Verschure P J, Van Noorden C J, Van Marle J, Van den Berg W B
Department of Rheumatology, University Hospital Nijmegen, The Netherlands.
Histochem J. 1996 Dec;28(12):835-57. doi: 10.1007/BF02331388.
Rheumatoid arthritis, a disease of unknown aetiology, is characterized by joint inflammation and, in its later stages, cartilage destruction. Inflammatory mediators may exert not only suppression of matrix synthesis but also cartilage degradation, which eventually leads to severe cartilage depletion. Systemically and locally produced growth factors and hormones regulate cartilage metabolism. Alterations in levels of these factors or in their activity can influence the pathogenesis of articular cartilage destruction in arthritic joints. The main topic of the present review is the role of the anabolic factor insulin-like growth factor-1 in the regulation of chondrocyte metabolic functions in normal and in diseased cartilage. This is the most important growth factor that balances chondrocytes proteoglycan synthesis and catabolism to maintain a functional cartilage matrix. A brief overview of how chondrocytes keep the cartilage matrix intact, and how catabolic and anabolic factors are thought to be involved in pathological cartilage destruction precedes the review of the role of this growth factor in proteoglycan metabolism in cartilage.
类风湿性关节炎是一种病因不明的疾病，其特征为关节炎症，在疾病后期会出现软骨破坏。炎症介质不仅可能抑制基质合成，还会导致软骨降解，最终导致严重的软骨损耗。全身和局部产生的生长因子及激素调节软骨代谢。这些因子水平或其活性的改变会影响关节炎关节中关节软骨破坏的发病机制。本综述的主要主题是合成代谢因子胰岛素样生长因子-1在正常和病变软骨中调节软骨细胞代谢功能的作用。这是平衡软骨细胞蛋白聚糖合成与分解代谢以维持功能性软骨基质的最重要生长因子。在综述该生长因子在软骨蛋白聚糖代谢中的作用之前，先简要概述软骨细胞如何保持软骨基质完整，以及分解代谢和合成代谢因子被认为如何参与病理性软骨破坏。
