代谢性骨性关节炎分子机制研究进展

被引：38

作者：

李盛华 ^{[1
]}

周明旺 ^{[1
]}

陈娴 ^{[2
]}

王金 ^{[2
]}

陈威 ^{[2
]}

柳海平 ^{[1
]}

机构：

[1] 甘肃省中医院

[2] 甘肃中医药大学

来源：

中国骨质疏松杂志 | 2016年 / 22卷 / 02期

关键词：

骨性关节炎; 代谢综合征; 分子机制;

D O I：

暂无

中图分类号：

R684.3 [关节炎];

学科分类号：

100220 [骨科学];

摘要：

传统观点认为骨性关节炎(osteoarthritis,OA)与衰老、创伤等因素有关,但越来越多的流行病学及生物学证据表明该病的发生与代谢综合征(metabolic syndrome,Met S)及其各组分等关系密切。本文将对该疾病的流行病学及基础研究进行综述,着重阐述其发生发展的分子生物学机制。其中,肥胖能引起脂肪细胞因子水平的异常,使关节内炎症因子和蛋白水解酶增多;高血糖导致的氧化应激、线粒体功能障碍、晚期糖基化终末产物堆积,使软骨细胞代谢稳态被打破;脂代谢异常造成的关节内炎症水平升高、细胞毒性增加、软骨细胞自噬活动减少;高血压使软骨下骨血流减少,使软骨下骨与软骨之间的生物学交流受到影响;"炎性衰老"不但是高血压与骨性关节炎共同的发病机制,也是二者相互影响的关键环节;某些微小RNA能对一些炎症因子,蛋白水解酶的表达进行调控,因而也在骨性关节炎的病理进程中起到了重要作用。本文通过对代谢性骨关节炎相关分子机制的研究,旨在为改善骨性关节炎的防治现状提供新靶点。

引用

页码：233 / 237

页数：5

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