The role of oxidative stress in placental-related diseases of pregnancy

被引:35
|
作者
Jauniaux, E. [1 ]
Burton, G. J. [2 ]
机构
[1] UCL, Acad Dept Obstet & Gynaecol, Inst Women Hlth, Sch Med, 86-96 Chenies Mews, London WC1E 6HX, England
[2] Univ Cambridge, Ctr Trophoblast Res, Dept Physiol Dev & Neurosci, Cambridge, England
关键词
Placenta; Oxygen; Oxidative stress; Miscarriage; Pre-eclampsia; Intra-uterine growth retardation (IUGR); SPIRAL ARTERIES; 1ST TRIMESTER; THREATENED MISCARRIAGE; SPONTANEOUS-ABORTION; CHORIONIC VILLI; PRE-ECLAMPSIA; BLOOD-FLOW; IN-VITRO; APOPTOSIS; 1ST-TRIMESTER;
D O I
10.1016/j.jgyn.2016.02.012
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
In normal pregnancies, the earliest stages of development take place in a low oxygen (O-2) environment. This physiological hypoxia of the early gestational sac protects the developing fetus against the deleterious and teratogenic effects of O-2 free radicals. Oxidative stress is manifested at the maternal fetal interface from early pregnancy onwards. In early pregnancy, a well-controlled oxidative stress plays a role in modulating placental development, functions and remodelling. Focal trophoblastic oxidative damage and progressive villous degeneration trigger the formation of the fetal membranes, which is an essential developmental step enabling vaginal delivery. Our data have demonstrated that the first trimester placenta in humans is histiotrophic and not haemochorial. The development and maintenance of a physiological O-2 gradient between the uterine and fetal circulations is also essential for placental functions, such as transport and hormonal synthesis. Pathological oxidative stress arises when the production of reactive O-2 species overwhelms the intrinsic anti-oxidant defences causing indiscriminate damage to biological molecules, leading to loss of function and cell death. We here review the role of oxidative stress in the pathophysiology of miscarriage, pre-eclampsia and fetal growth restriction. (C) 2016 Elsevier Masson SAS. All rights reserved.
引用
收藏
页码:775 / 785
页数:11
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