Connecting G protein-coupled estrogen receptor biomolecular mechanisms with the pathophysiology of preeclampsia: a review.
Connecting G protein-coupled estrogen receptor biomolecular mechanisms with the pathophysiology of preeclampsia: a review.
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DOI：
10.1186/s12958-023-01112-7
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发表时间：
2023-07-01
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影响因子：
--
通讯作者：
中科院分区：
文献类型：
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在整个妊娠过程中，与胎儿组织接触的小母体螺旋动脉经历结构重塑，失去平滑肌细胞，对血管收缩剂的反应变差。此外，胎盘绒毛外滋养层细胞侵入母体蜕膜，以建立胎儿胎盘绒毛与母体血液供应之间的相互作用。当成功时，这个过程使氧气，营养物质和信号分子的运输成为可能，但不足会导致胎盘缺血。作为回应，胎盘释放血管活性因子，进入母体循环并促进母体心肾功能障碍，这是先兆子痫（PE）的标志，是母体和胎儿死亡的主要原因。在PE的发展中，一个未充分研究的机制是通过G蛋白偶联雌激素受体（GPER）的膜启动的雌激素信号传导的影响。最近的证据表明，GPER激活与正常滋养层浸润，胎盘血管生成/缺氧，子宫胎盘血管舒张的调节，这些机制可以解释部分雌激素诱导的控制子宫重塑和胎盘发育在怀孕。虽然GPER在PE中的相关性仍然是推测性的，但本文综述了我们目前对GPER刺激如何调节正常妊娠的一些特征及其信号网络与PE中子宫胎盘功能障碍之间的潜在联系的理解。综合这些信息将有助于开发创新的治疗方案。
Throughout the course of pregnancy, small maternal spiral arteries that are in contact with fetal tissue undergo structural remodeling, lose smooth muscle cells, and become less responsive to vasoconstrictors. Additionally, placental extravillous trophoblasts invade the maternal decidua to establish an interaction between the fetal placental villi with the maternal blood supply. When successful, this process enables the transport of oxygen, nutrients, and signaling molecules but an insufficiency leads to placental ischemia. In response, the placenta releases vasoactive factors that enter the maternal circulation and promote maternal cardiorenal dysfunction, a hallmark of preeclampsia (PE), the leading cause of maternal and fetal death. An underexplored mechanism in the development of PE is the impact of membrane-initiated estrogen signaling via the G protein-coupled estrogen receptor (GPER). Recent evidence indicates that GPER activation is associated with normal trophoblast invasion, placental angiogenesis/hypoxia, and regulation of uteroplacental vasodilation, and these mechanisms could explain part of the estrogen-induced control of uterine remodeling and placental development in pregnancy. Although the relevance of GPER in PE remains speculative, this review provides a summary of our current understanding on how GPER stimulation regulates some of the features of normal pregnancy and a potential link between its signaling network and uteroplacental dysfunction in PE. Synthesis of this information will facilitate the development of innovative treatment options.
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影响因子：
3.7
作者：
Dechanet C;Fort A;Barbero-Camps E;Dechaud H;Richard S;Virsolvy A
通讯作者：
Virsolvy A
DOI：
10.1136/bmj.f6564
发表时间：
2013-11-07
期刊：
BMJ (Clinical research ed.)
影响因子：
--
作者：
Ananth CV;Keyes KM;Wapner RJ
通讯作者：
Wapner RJ
影响因子：
7.2
作者：
通讯作者：
--
影响因子：
9.8
作者：
Brosens, Ivo;Brosens, Jan J.;Benagiano, Giuseppe
通讯作者：
Benagiano, Giuseppe
影响因子：
1.2
作者：
Cheng, Ching-Yi;Hsieh, Hsi-Lung;Yang, Chuen-Mao
通讯作者：
Yang, Chuen-Mao