Molecular mechanisms of cartilage remodelling in osteoarthritis
Molecular mechanisms of cartilage remodelling in osteoarthritis
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DOI：
10.1016/j.biocel.2010.06.022
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发表时间：
2010-10-01
影响因子：
4
通讯作者：
Pap，Thomas
中科院分区：
文献类型：
--
作者：
Bertrand，Jessica;Cromme，Christoph;Pap，Thomas
骨关节炎（OA）是一种退行性关节疾病，其主要特征是关节软骨的进行性破坏。蛋白聚糖的丧失，细胞外基质（ECM）的矿化和软骨细胞的肥厚分化构成了该疾病的标志。OA的发病机制包括几种途径，其中单个途径的研究很好，部分了解，但其复杂的相互作用仍不清楚。这篇综述总结了最近关于潜在机制的数据，特别是关于细胞-基质相互作用和软骨矿化。它指出了为什么这些发现对未来OA研究和开发新的OA治疗策略具有重要意义。
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.