Endoplasmic reticulum stress in the pathogenesis of early-onset pre-eclampsia.
Endoplasmic reticulum stress in the pathogenesis of early-onset pre-eclampsia.
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DOI：
10.1016/j.preghy.2010.12.002
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发表时间：
2011-01
影响因子：
2.2
通讯作者：
Yung, Hong-Wa
中科院分区：
文献类型：
--
作者：
Burton, Graham J.;Yung, Hong-Wa
最近的数据提供了高水平的内质网应激的分子证据，在非劳动胎盘早发型先兆子痫的情况下。内质网应激与氧化应激密切相关，两者通常具有相同的病因。在先兆子痫的情况下，这可能是胎盘灌注不良，继发于螺旋动脉转换不足。内质网应激激活了许多旨在恢复体内平衡的信号通路，但如果这些尝试失败，那么凋亡机制可能被激活。胎盘发育和功能的潜在后果是多种多样的。蛋白质合成的抑制导致参与细胞周期控制的许多激酶、生长因子和调节蛋白的水平降低，并且体外实验揭示内质网应激减缓细胞增殖。因此，在第二和第三孕期的慢性低水平压力可能导致生长受限表型。更高水平的内质网应激导致促炎途径的激活，这是先兆子痫的一个特征，可能有助于母体内皮细胞激活。这些发现强调了细胞对压力反应的复杂性，以及在考虑治疗干预时以整体方式处理这些问题的必要性。
Recent data have provided molecular evidence of high levels of endoplasmic reticulum stress in non-laboured placentas from cases of early-onset pre-eclampsia. Endoplasmic reticulum stress is intricately linked to oxidative stress, and the two often share the same aetiology. In the case of pre-eclampsia this is likely to be placental malperfusion, secondary to deficient conversion of the spiral arteries. Endoplasmic reticulum stress activates a number of signalling pathways aimed at restoring homeostasis, but if these attempts fail then the apoptotic machinery may be activated. The potential consequences for placental development and function are numerous and diverse. Inhibition of protein synthesis results in lower levels of many kinases, growth factors and regulatory proteins involved in cell cycle control, and experiments in vitro reveal that endoplasmic reticulum stress slows cell proliferation. Chronic, low levels of stress during the second and third trimesters may therefore result in a growth restricted phenotype. Higher levels of endoplasmic reticulum stress lead to activation of pro-inflammatory pathways, a feature of pre-eclampsia that may contribute to maternal endothelial cell activation. These findings emphasise the complexity of cellular responses to stress, and the need to approach these in a holistic fashion when considering therapeutic interventions.
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影响因子：
56.9
作者：
HWANG, C;SINSKEY, AJ;LODISH, HF
通讯作者：
LODISH, HF
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：
7.8
作者：
Hitomi, Junichi;Katayama, Taiichi;Eguchi, Yutaka;Kudo, Takashi;Taniguchi, Manabu;Koyama, Yoshihisa;Manabe, Takayuki;Yamagishi, Satoru;Bando, Yoshio;Imaizumi, Kazunori;Tsujimoto, Yoshihide;Tohyama, Masaya
通讯作者：
Tohyama, Masaya
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