MAPK1/ERK2通过SRF调控中性粒细胞弹性蛋白酶分泌在子痫前期发病中的研究进展

子痫前期是一种累及全身多脏器的妊娠期特发性疾病,是导致孕产妇及围生儿死亡的主要原因。发病机制包括过度氧化应激、炎症免疫过度激活、内皮细胞功能障碍等,其中中性粒细胞过度活化释放弹性蛋白酶,导致血管内皮细胞损伤是关键环节。研究发现子痫前期患者中性粒细胞中丝裂原活化蛋白激酶1(MAPK1)及中性粒细胞弹性蛋白酶(NE)水平显著升高。血清反应因子(SRF)是MAPK1途径下游靶蛋白,使活化的中性粒细胞黏附和迁移,导致内皮细胞损伤。MAPK1可能通过调控SRF从而导致中性粒细胞过度活化释放NE从而参与子痫前期的发病。本文将对MAPK1通过SRF调控NE分泌的相关作用机制进行综述。

Research Progress of MAPK1/ERK2 Regulating Neutrophil Elastase Secretion through SRF in the Pathogenesis of Pre-Eclampsia

Pre-eclampsia(PE) is a gestational idiopathic disease involving multiple organs of the body and one of the leading causes of maternal and perinatal death. The mechanism includes excessive oxidative stress, excessive activation of inflammation and immune system, and dysfunction of vascular endothelial, etc. Among them, the key link is that neutrophils over-activate and release elastase, leading to damage of vascular endothelial cells. It was found that levels of mitogen-activated protein kinase 1(MAPK1) and neutrophil elastase(NE) were significantly increased in neutrophils of PE. Serum response factors(SRF) are downstream target proteins of MAPK1 pathway, which cause adhesion and migration of activated neutrophils and damage of endothelial cells. MAPK1 may be involved in the pathogenesis of PE by regulating SRF and thereby leading to the over-activation of neutrophils and the release of NE. The mechanism of MRPK1 regulating NE secretion through SRF will be reviewed in this paper.