摘要
肺纤维化是各种慢性肺部疾病最终的共同通路,且最终结局为特发性肺纤维化。其特征是肺泡上皮细胞损伤/活化,成纤维细胞/肌纤维母细胞的大量增殖,及细胞外基质(extracellular matrix,ECM)过度沉积,最终导致肺实质的破坏。基质金属蛋白酶(matrix metalloproteinases,MMPs)是体内重要的水解酶系,能降解大多数ECM的成分,但其活性可被其特异性抑制剂——基质金属蛋白酶组织抑制剂(tissue inhibitors of metalloproteinases,TIMPs)所抑制。MMPs与TIMPs在肺纤维化的发生、发展过程中存在动态变化。肺纤维化的发生可能与MMPs与TIMPs之间失衡导致的ECM反复破坏、修复、重构与过度沉积有关。
Pulmonary fibrosis is the final common pathway of a large variety of chronic lung disease,and idiopathic pulmonary fibrosis（IPF）is the most aggressive form.IPF is characterized by alveolar epithelial cell injury/activation,myofibroblast/fibroblast proliferation,and excessive accumulation of extracellular matrix（ECM）,which ultimately results in the destruction of lung parenchyma.Matrix metalloproteinases（MMPs）are important hydrolysis enzymes that can degrade most of the ECM.However,the activity of MMPs may be inhibited by its specific inhibitors tissue inhibitors of metalloproteinases（TIMPs）.Dynamic changes in MMPs and TIMPs have been shown in the occurrence and development of pulmonary fibrosis,which may be correlated with the repeated destruction,repair,reconstruction and excessive deposition of ECM caused by the imbalance of MMPs and TIMPs.
出处
《南昌大学学报（医学版）》
CAS
2015年第1期88-91,100,共5页
Journal of Nanchang University：Medical Sciences
关键词
特发性肺纤维化
基质金属蛋白酶
基质金属蛋白酶组织抑制剂
细胞外基质
机制
idiopathic pulmonary fibrosis
matrix metalloproteinases
tissue inhibitors of metalloproteinases
extracellular matrix
mechanism
