基质金属蛋白酶降解胞外基质致未足月胎膜早破研究进展

早产是威胁围生儿生命健康的首要病因。据统计,2012年中国早产发生率为8.1%。未足月胎膜早破(preterm premature rupture of membranes,PPROM)占早产的25%~30%,重要诱因为宫内感染。近年研究发现,PPROM的分子机制为胎膜组织中胞外基质过早降解,主要由基质金属蛋白酶(matrix metalloproteinases,MMPs)在胎膜组织中的激活引起。MMPs的激活原因有炎症因子的表达增高,如白细胞介素1(IL-1),IL-6以及肿瘤坏死因子α(TNF-α),但具体机制尚有待研究。MMPs在正常分娩与PPROM发生过程中的激活、分泌及其影响因素仍需探索,其可能作为预测妊娠结局的标记物,为PPROM的预防与治疗提供突破点。

Research Progress of Matrix Metalloproteinases in Preterm Premature Rupture of Membranes through Degrading Extracellular Matrix

Preterm birth is the first critical factor of life, threatening diseases for the perinatal. According to the statistics, the preterm birth rate in China reached 8.1%in 2012. And the frequency of preterm premature rupture of membranes (PPROM) is about 25%-30%, and intrauterine infection is the principal element. The recent research shows that a molecular mechanism of PPROM is advanced degradation of extracellular matrix, which due to the activation of matrix metalloproteinases (MMPs) in fetal membrane. The high expression of cytokines, such as IL-1, IL-6 and TNF-α, maybe the reason of MMPs′activation. The process of activation and secretion of MMPs in term labor and preterm birth still need to be explored, which may be considered as a marker of pregnancy outcome. MMPs can provide a breakpoint of prevention and therapy for PPROM.