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SIRT6、MMPs与胎膜早破的相关性研究
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Abstract:
胎膜早破(PROM)指的是孕妇在临产前胎膜出现的自发性破裂，是产科常见的并发症之一。已知胎膜的抗张力作用/拉伸强度主要由羊膜细胞外基质(ECM)中的胶原含量决定的,而基质金属蛋白酶(MMPs)是降解ECM成分的强效酶家族，在炎性因子的作用下可使其在胎膜组织中的表达含量增加，从而导致局部胎膜变薄弱甚至PROM的发生。SIRT6是一种NAD+依赖性蛋白脱乙酰酶，可使NF-κB的RelA亚单位去乙酰化，抑制其目标启动子，抑制细胞凋亡和细胞衰老，其也可通过共价修饰参与炎症反应、氧化应激等在内的细胞内生理活动，且可通过调控MMPs表达水平来影响胎膜的完整性，进而致使PROM的发生。本文就SIRT6、MMPs与PROM的相关性进行综述，期望对PROM的发生机制以及防治有更进一步的认识。
Premature rupture of fetal membrane (PROM) refers to spontaneous rupture of fetal membrane in pregnant women before labor, which is one of the common complications in obstetrics. It is known that the anti-tension effect/tensile strength of the fetal membrane is mainly determined by the col-lagen content in the amniotic extracellular matrix (ECM), and matrix metalloproteinases (MMPs) are powerful enzymes that degrade ECM components. Under the action of inflammatory factors, the expression of MMPS in the fetal membrane tissue can be increased, resulting in local weakening of the fetal membrane and even the occurrence of PROM. SIRT6 is an NAD+ dependent protein deacetylase, which can deacetylate the RelA subunit of NF-κB, inhibit its target promoter, inhibit apoptosis and cell senescence, and participate in intracellular physiological activities including in-flammation and oxidative stress through covalent modification, and affect the integrity of fetal membrane by regulating the expression level of MMPs. And that leads to PROM. In this paper, the correlation between SIRT6, MMPs and PROM was reviewed, hoping to have a further understanding of the mechanism and prevention of PROM.
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