Yasuda Tadashi
Department of Sports Medicine, Tenri University, 80 Tainosho-cho, Tenri, 632-0071, Japan.
Mod Rheumatol. 2006;16(4):197-205. doi: 10.1007/s10165-006-0490-6.
The progressive destruction of articular cartilage is one of the hallmarks of osteoarthritis and rheumatoid arthritis. Cartilage degradation is attributed to different classes of catabolic factors, including proinflammatory cytokines, aggrecanases, matrix metalloproteinases, and nitric oxide. Recently, matrix degradation products generated by excessive proteolysis in arthritis have been found to mediate cartilage destruction. These proteolytic fragments activate chondrocytes and synovial fibroblasts via specific cell surface receptors that can stimulate catabolic intracellular signaling pathways, leading to the induction of such catalysts. This review describes the catabolic activities of matrix degradation products, especially fibronectin fragments, and discusses the pathologic implication in cartilage destruction in osteoarthritis and rheumatoid arthritis. Increased levels of these degradation products, found in diseased joints, may stimulate cartilage breakdown by mechanisms of the kind demonstrated in the review.
关节软骨的进行性破坏是骨关节炎和类风湿关节炎的标志之一。软骨降解归因于不同种类的分解代谢因子，包括促炎细胞因子、聚集蛋白聚糖酶、基质金属蛋白酶和一氧化氮。最近发现，关节炎中过度蛋白水解产生的基质降解产物可介导软骨破坏。这些蛋白水解片段通过特定的细胞表面受体激活软骨细胞和滑膜成纤维细胞，这些受体可刺激分解代谢的细胞内信号通路，导致此类催化剂的诱导。本文综述了基质降解产物，特别是纤连蛋白片段的分解代谢活性，并讨论了其在骨关节炎和类风湿关节炎软骨破坏中的病理意义。在患病关节中发现的这些降解产物水平升高，可能通过本文所述的机制刺激软骨破坏。
