代谢性骨性关节炎分子机制研究进展

发布时间：2018-02-09 05:41

本文关键词： 骨性关节炎代谢综合征分子机制　出处：《中国骨质疏松杂志》2016年02期 　论文类型：期刊论文

【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。
[Abstract]:The traditional view is that osteoarthritis (OAA) is related to aging, trauma and other factors. However, more and more epidemiological and biological evidence have shown that the occurrence of the disease is closely related to metabolic syndromedromedromedromedromedromedromedromedromedromedromedromedromedromedromedromedromedromedromes (Met) and its components. Among them, obesity can cause abnormal levels of adipocyte cytokines, increase inflammatory factors and proteolytic enzymes in joints, oxidative stress induced by hyperglycemia, and dysfunction of mitochondria. The accumulation of advanced glycation end products broke the homeostasis of chondrocyte metabolism, increased the level of intra-articular inflammation, increased cytotoxicity and decreased autophagy of chondrocytes caused by abnormal lipid metabolism, and decreased the blood flow of subchondral bone due to hypertension. "inflammatory aging" is not only a common pathogenesis of hypertension and osteoarthritis, but also a key link in the interaction between them. The expression of proteolytic enzymes plays an important role in the pathological process of osteoarthritis. To provide a new target for improving the prevention and treatment of osteoarthritis.
【作者单位】：甘肃省中医院;甘肃中医药大学;
【基金】：国家自然科学基金(81260546) 甘肃省青年科技基金计划(1208RJYA041) 甘肃省自然科学基金项目(1107RJZA235)
【分类号】：R684.3

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