摘要年龄相关性黄斑变性(AMD)是导致老年人中心视力丧失的主要视网膜疾病之一,其发病机制目前尚未完全清楚.近年来的临床研究和基础研究表明,受基质金属蛋白酶(MMPs)和组织金属蛋白酶抑制剂(TIMPs)调控的细胞外基质(ECM)的代谢障碍在AMD的发病过程中起重要作用.研究表明,MMPs与TIMPs平衡的失调导致Bruch膜不同的病理性改变,参与玻璃膜疣的形成,调控脉络膜新生血管(CNV)的形成；而ECM降解产物弹性蛋白衍生肽(EDPs)的水平反映了MMPs水平及其活性,EDPs水平的升高可增加早期AMD向新生血管性AMD转化的风险.就MMPs和TIMPs及ECM降解产物EDPs在AMD发病机制中的研究进展进行综述.

abstractsAge-related maculadegeneration (AMD) ione of majoretinal diseaseleading to central vision loss.Apresent,the pathogenesiof AMD ibelow understood.Ovethe pasdecade years,dysmetabolism of extracellulamatrix (ECM) regulated by matrix metalloproteinase(MMPs) and tissue inhibitoof metalloproteinase(TIMPs) system play an importanrole in the pathogenesiof AMD.The imbalance of MMPand TIMPleadto differenpathological changeof Bruch 'membrane,which involvein drusen formation and regulatechoroidal neovascularization (CNV).The level of elastin-derived peptides(EDPs) reflectthe level and activity of M MPs,and the elevated level of EDPincreasethe risk of early AMD to advance neovasculaAMD.Thiarticle reviewthe research progression of MMPs,TIMPand the elastin-derived peptideand in AMD.