基质金属蛋白酶与慢性阻塞性肺疾病的相关研究进展  

Research Progress of Matrix Metalloproteinase and Chronic Obstructive Pulmonary Disease

作　　者：王鸿伦 吕美玉 强丽霞[1] 商行 张亮[1] 金寿德[1] WANG Honglun;LYU Meiyu;QIANG Lixia;SHANG Hang;ZHANG Liang;JIN Shoude(Department of Respiratory Medicine,the Fourth Hospital of Harbin Medical University,Harbin 150001,China)

机构地区：[1]哈尔滨医科大学附属第四医院呼吸内科,哈尔滨150001

出　　处：《医学综述》2022年第4期638-642,共5页Medical Recapitulate

基　　金：国家自然科学基金(81670028);黑龙江省自然科学基金(YQ2019H011)。

摘　　要：慢性阻塞性肺疾病(COPD)是一种以不可逆性气流受限为特征且肺功能呈进行性下降的慢性气道疾病。蛋白酶-抗蛋白酶失衡是COPD的主要发病机制之一,基质金属蛋白酶(MMP)在气道、肺组织结构的破坏中起关键作用,可调节炎症因子的表达,参与患者气道重构进程。MMP还可通过降解细胞外基质的多种成分调节细胞的生长、分化及损伤修复。蛋白酶的数量和活性超过抗蛋白酶的抑制作用可导致细胞外基质被大量降解,从而促进COPD的发展。此外,MMP的基因多态性也可影响COPD患者的病程进展,Toll样受体、Wnt信号通路和核因子κB均可通过调节MMP的产生与释放参与气道重构和炎症反应。因此,深入研究MMP与COPD关系可以为COPD患者的治疗提供新思路。Chronic obstructive pulmonary disease(COPD)is a chronic airway disease characterized by irreversible airflow limitation and progressive lung dysfunction.The protease-antiprotease imbalance is a major pathogenesis of COPD.Matrix metalloproteinase(MMP)play a key role in the destruction of the airway and lung tissue structure,as they can regulate the expression of inflammatory factors and participate in the process of airway remodeling in the patients.MMP can also regulate cell growth,differentiation and injury repair by degrading multiple components of the extracellular matrix.When the quantity and activity of proteases exceed the inhibition of antiproteases,it causes the extracellular matrix to be massively degraded,which promotes the development of COPD.In addition,gene polymorphisms of MMP can also influence the progression of COPD,and Toll like receptors,Wnt signal pathway and nuclear factors-κB can participate in airway remodeling and inflammatory responses by regulating the production and release of MMP.Therefore,in-depth studies of the relationship between MMP and COPD can provide new ideas for the treatment of COPD.

关 键 词：慢性阻塞性肺疾病 基质金属蛋白酶 蛋白酶-抗蛋白酶失衡 气道重构 损伤修复 

分 类 号：R563.9[医药卫生—呼吸系统]