Placental endoplasmic reticulum stress and oxidative stress in the pathophysiology of unexplained intrauterine growth restriction and early onset preeclampsia.
Placental endoplasmic reticulum stress and oxidative stress in the pathophysiology of unexplained intrauterine growth restriction and early onset preeclampsia.
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DOI：
10.1016/j.placenta.2008.11.003
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发表时间：
2009-03
期刊：
影响因子：
3.8
通讯作者：
Charnock-Jones DS
中科院分区：
文献类型：
--
作者：
Burton GJ;Yung HW;Cindrova-Davies T;Charnock-Jones DS
不明原因的宫内生长受限和早发性先兆子痫的妊娠并发症被认为是继发于母体螺旋动脉转换不足的胎盘灌注不良的共同病因。一个关键的问题是，这些不同的临床表现是否反映了不同的胎盘病理，还是由于孕妇对来自胎盘的共同因素的反应发生了变化。最近，内质网应激继发的蛋白质合成抑制的分子证据为这两种情况下的小胎盘表型提供了解释。然而，由更严重的内质网应激激活的其他途径仅在与早发性子痫前期相关的妊娠胎盘中观察到。在这里，我们回顾文献，并得出结论，在这些病例中，有证据表明母体血管对胎盘的损害更大。我们推测，在血压正常的宫内生长受限病例中，胎盘病理主要集中在内质网应激，而在合并先兆子痫的病例中，氧化应激进一步叠加。这会导致促炎细胞因子、抗血管生成因子和滋养细胞无坏死碎片的有效混合物释放到母体循环中，从而导致外周综合征。母体和胎儿的体质因素可能会调节胎盘对母体血管损伤的反应，以及母亲如何受到胎盘因子释放的影响。然而，主要结论是，这两种情况的区别在于螺旋动脉转换起始缺陷的严重程度，以及由此导致的胎盘内质网应激和氧化应激的相对程度。
The pregnancy complications of unexplained intrauterine growth restriction and early onset preeclampsia are thought to share a common aetiology in placental malperfusion secondary to deficient maternal spiral artery conversion. A key question is whether the contrasting clinical manifestations reflect different placental pathologies, or whether they are due to altered maternal responses to a common factor derived from the placenta. Recently, molecular evidence of protein synthesis inhibition secondary to endoplasmic reticulum stress has provided an explanation for the small placental phenotype in both conditions. However, other pathways activated by more severe endoplasmic reticulum stress are only observed in placentas from pregnancies associated with early onset preeclampsia. Here, we review the literature and conclude that there is evidence of greater maternal vascular compromise of the placenta in these cases. We speculate that in cases of normotensive intrauterine growth restriction the placental pathology is centred predominantly around endoplasmic reticulum stress, whereas in cases complicated by preeclampsia oxidative stress is further superimposed. This causes the release of a potent mix of pro-inflammatory cytokines, anti-angiogenic factors and trophoblastic aponecrotic debris into the maternal circulation that causes the peripheral syndrome. Maternal and fetal constitutional factors may modulate how the placenta responds to the maternal vascular insult, and how the mother is affected by the placental factors released. However, the principal conclusion is that the difference between these two conditions lies in the severity of the initiating deficit in spiral arterial conversion, and the relative degrees of endoplasmic reticulum stress and oxidative stress induced in the placenta as a result.
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核因子-kappa B、p38 和应激激活蛋白激酶丝裂原激活蛋白激酶信号通路调节人胎盘外植体中的促炎细胞因子和细胞凋亡，以响应氧化应激：抗氧化维生素的作用。
影响因子：
6
作者：
Cindrova-Davies, Tereza;Spasic-Boskovic, Olivera;Jauniaux, Eric;Charnock-Jones, D. Stephen;Burton, Graham J.
通讯作者：
Burton, Graham J.
影响因子：
9.8
作者：
Choi, Suk-Joo;Oh, Soo-young;Roh, Cheong-Rae
通讯作者：
Roh, Cheong-Rae
DOI：
10.1111/j.1471-0528.1981.tb02222.x
发表时间：
1981-01-01
期刊：
BRITISH JOURNAL OF OBSTETRICS AND GYNAECOLOGY
影响因子：
--
作者：
GERRETSEN, G;HUISJES, HJ;ELEMA, JD
通讯作者：
ELEMA, JD
DOI：
10.1046/j.1525-1373.1999.d01-139.x
发表时间：
1999-12-01
影响因子：
--
作者：
Hubel, CA
通讯作者：
Hubel, CA
影响因子：
3.8
作者：
Cindrova-Davies, T.
通讯作者：
Cindrova-Davies, T.