MMP13在骨关节炎发病机制中的研究进展  

Research progress on MMP13 in the pathogenesis of osteoarthritis

作　　者：马崇文 张小辉 杨信信 阎亮 李睿[1] 夏亚一[1] MA Chong-wen;ZHANG Xiao-hui;YANG Xinxin;YAN Liang;LI Rui;XIA Ya-yi(Orthopaedic Department,The Second Hospital of Lanzhou University,Gansu Key Laboratory of Orthopaedics,Lanzhou730000 ,China)

机构地区：[1]兰州大学第二医院骨科甘肃省骨关节疾病研究重点实验室

出　　处：《中国矫形外科杂志》2019年第19期1773-1776,共4页Orthopedic Journal of China

基　　金：兰州市科技计划项目(编号：2017-4-88);国家自然科学基金面上项目(编号：81672207;81874107);甘肃省青年科技基金计划项目(编号：1506RJYA200);甘肃省自然科学基金面上项目(编号：17JR5RA188);中央高校课题(编号：LZUJBKY-2018-KB16)

摘　　要：骨关节炎(OA)是一种影响大量人群的退行性关节疾病,这种疾病的机制研究处于热点阶段。基质金属蛋白酶(MMP)-13由于其对切割II型胶原的特异性而在软骨重塑和降解中具有关键的限速功能,可通过多种方式和多条通路调节骨骼发育和骨重建。本文就MMP13在骨关节炎中的调控、相关信号通路以及临床研究的进展进行综述。Osteoarthritis (OA) is a degenerative joint disease that affects a large number of people. The mechanism of this highly prevalent disease is still at a hot point of research. Matrix metalloproteinase (MMP)-13 has critical roles in cartilage re modeling and degradation due to its specific cutting of type II collagen. In addition, the MMP-13 also regulates skeletal develop ment and bone remodeling in a variety of ways and multiple pathways. This article reviews the regulation of MMP13 in osteoar thritis, related signaling pathways, and advances in clinical research.

关 键 词：骨关节炎 MMP13 调节机制 信号通路 

分 类 号：R318[医药卫生—生物医学工程]