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作 者:胡悦 盛红娜[1] 梁美育 范卓然 华绍芳[1] HU Yue;SHENG Hong-na;LIANG Mei-yu;FAN Zhuo-ran;HUA Shao-fang(Department of Obstetrics,The Second Hospital of Tianjin Medical University,Tianjin 300211,China)
出 处:《国际妇产科学杂志》2023年第6期695-698,共4页Journal of International Obstetrics and Gynecology
基 金:天津医科大学第二医院青年科研基金(2021ydey06)。
摘 要:子痫前期(pre-eclampsia,PE)是一种以高血压和多系统器官功能受累为特征的妊娠特异性综合征,虽然其具体发病机制尚不明确,但胎盘形成时期滋养细胞侵袭过浅或受限而导致的胎盘灌注不足、持续缺氧可能是重要的初始事件。作为胎盘分泌的重要类固醇激素,雌激素通过雌激素受体(estrogen receptor,ER)、雌激素反应元件(estrogen response element,ERE)信号通路的基因组或非基因组效应调控靶基因表达水平,致使滋养细胞增殖、凋亡和侵袭等生物学行为发生改变,还可能介导子宫内膜蜕膜化缺失从而参与胎盘浅着床、灌注不足的发生。雌激素及其信号通路还可通过调节一氧化氮等血管活性因子水平及有关离子通道活性,调节子宫动脉平滑肌的舒缩能力,通过多种机制参与PE、复发性流产等高危妊娠的发生和发展。Pre-eclampsia(PE)is a pregnancy specific syndrome characterized by hypertension and multiple organ dysfunction.Although the specific pathogenesis is not yet clear,insufficient placental perfusion and persistent hypoxia caused by shallow and limited invasion of trophoblasts during placental formation may be important initial events.As an important steroid hormone secreted by the placenta,estrogen regulates target gene expression levels through genomic or non-genomic effects of estrogen receptor(ER)and estrogen response element(ERE)signaling pathways,leading to changes in biological behaviors such as trophoblast proliferation,apoptosis,invasion,and possibly mediating the loss of endometrial decidualization,thereby participating in placental shallow implantation and the occurrence of insufficient perfusion.Estrogen and its signaling pathways can also regulate the levels of vasoactive factors such as nitric oxide and the activity of related ion channels to regulate the contractile and relaxing ability of uterine artery smooth muscle,and participate in the occurrence and development of high-risk pregnancies such as PE and recurrent spontaneous abortion through various mechanisms.
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