摘要
保留关节软骨是保护滑膜关节免于成为骨关节炎(OA)关节的有效方法。了解关节软骨变性的分子基础将为开发软骨保存药物提供有价值的信息。当前,尚无可用于在OA发生过程中预防关节软骨破坏的疾病缓解OA药物(DMOAD)。当前用于OA的药物治疗集中于减轻疾病晚期的关节疼痛,肿胀和炎症。但是,根据过去15到20年间几个独立研究实验室和我们实验室的发现,我们相信我们对关节软骨变性具有功能性分子的理解。在这篇综述文章中,我们介绍并讨论实验证据,以证明关节软骨退化的分子事件的顺序链,该分子链由转化生长因子β1,高温需求A1(丝氨酸蛋白酶),盘状蛋白结构域受体2(天然纤维胶原蛋白的细胞表面受体酪氨酸激酶)和基质金属蛋白酶13(一种细胞外基质降解酶)。如我们强烈怀疑的那样,如果该分子途径负责引发和加速关节软骨变性,最终导致进行性关节衰竭,那么这些分子可能是DMOADs发育的理想治疗靶标。
关键词: TGF-β1,HTRA1,DDR2,MMP-13,关节软骨,变性,骨关节炎。
图形摘要
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