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骨关节炎中软骨重塑的分子机制。

Molecular mechanisms of cartilage remodelling in osteoarthritis.

机构信息

Institute of Experimental Musculoskeletal Medicine IEMM, University Hospital Muenster, Muenster, Germany.

出版信息

Int J Biochem Cell Biol. 2010 Oct;42(10):1594-601. doi: 10.1016/j.biocel.2010.06.022. Epub 2010 Jul 9.

Abstract

Osteoarthritis (OA) is a degenerative joint disease that is characterized primarily by progressive breakdown of articular cartilage. The loss of proteoglycans, the mineralization of the extracellular matrix (ECM) and the hypertrophic differentiation of the chondrocytes constitute hallmarks of the disease. The pathogenesis of OA includes several pathways, which in single are very well investigated and partly understood, but in their complex interplay remain mainly unclear. This review summarises recent data on the underlying mechanisms, specifically with respect to cell-matrix interactions and cartilage mineralization. It points out why these findings are of importance for future OA research and for the development of novel therapeutic strategies to treat OA.

摘要

骨关节炎(OA)是一种退行性关节疾病,主要表现为关节软骨的进行性破坏。蛋白聚糖的丢失、细胞外基质(ECM)的矿化和软骨细胞的肥大分化是该疾病的特征标志。OA 的发病机制包括几个途径,其中每个途径都有很好的研究和部分理解,但在其复杂的相互作用中仍然主要不清楚。这篇综述总结了关于潜在机制的最新数据,特别是关于细胞-基质相互作用和软骨矿化的机制。它指出了为什么这些发现对未来的 OA 研究和开发治疗 OA 的新的治疗策略具有重要意义。

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