Dysregulated complement activation as a common pathway of injury in preeclampsia and other pregnancy complications.
Dysregulated complement activation as a common pathway of injury in preeclampsia and other pregnancy complications.
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DOI：
10.1016/j.placenta.2010.03.010
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发表时间：
2010-07
期刊：
影响因子：
3.8
通讯作者：
Salmon, J. E.
中科院分区：
文献类型：
--
作者：
Lynch, A. M.;Salmon, J. E.
补体系统保护宿主免受入侵生物体的侵害，引发炎症并处理免疫复合物和炎性损伤的产物。补体系统提供了先天性和适应性免疫系统之间的重要联系。实验观察表明，增加的补体激活导致和/或延续妊娠期间的炎症。最近的研究表明补体激活和先兆子痫之间的联系。补体的过度激活或调节不足可募集白细胞，并释放与先兆子痫特征性胎盘功能不全和母体内皮功能障碍相关的强效炎症和抗血管生成介质。我们回顾了动物和人类的研究，链接补体激活和先兆子痫的致病事件，目前的证据表明，补体系统的激活与先兆子痫的发展，并提供了新的目标，以防止其并发症。
The complement system protects the host against invading organisms, initiates inflammation and dispose of immune complexes and the products of inflammatory injury. The complement system provides an important link between the innate and adaptive immune systems. Experimental observations suggest that increased complement activation causes and/or perpetuates inflammation during pregnancy. Recent studies suggest a link between complement activation and preeclampsia. Excessive activation or insufficient regulation of complement recruits leukocytes and unleashes potent inflammatory and anti-angiogenic mediators associated with placental insufficiency and maternal endothelial dysfunction characteristic of preeclampsia. We review the animal and human studies that link complement activation and pathogenic events in preeclampsia, present evidence that activation of the complement system is associated with the development of preeclampsia and provides new targets to prevent its complications.
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DOI：
10.1111/j.1600-0897.1992.tb00787.x
发表时间：
1992-10-01
影响因子：
3.6
作者：
ABRAMSON, SB;BUYON, JP
通讯作者：
BUYON, JP
影响因子：
3.8
作者：
Cindrova-Davies, T.
通讯作者：
Cindrova-Davies, T.
影响因子：
5.9
作者：
BUYON, JP;CRONSTEIN, BN;WEISSMANN, G
通讯作者：
WEISSMANN, G
影响因子：
--
作者：
BUYON, JP;TAMERIUS, J;ABRAMSON, SB
通讯作者：
ABRAMSON, SB
影响因子：
20.3
作者：
Fremeaux-Bacchi, Veronique;Miller, Elizabeth C.;Atkinson, John P.
通讯作者：
Atkinson, John P.