Oxidative stress in the pathogenesis of preeclampsia
Oxidative stress in the pathogenesis of preeclampsia
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DOI：
10.1046/j.1525-1373.1999.d01-139.x
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发表时间：
1999-12-01
影响因子：
--
通讯作者：
Hubel, CA
中科院分区：
文献类型：
--
作者：
Hubel, CA
妊娠综合征先兆子痫的病因和发病机制仍然知之甚少。大量证据表明，先兆子痫的多种表现，包括血管反应性改变、血管痉挛和许多器官系统中的离散病理学，源自母体血管内皮内的病理变化。本文以内皮细胞功能障碍为主题，重点综述氧化应激失衡在子痫前期发病机制中的作用，包括：1）胎盘在子痫前期中的作用; 2）氧化应激在子痫前期胎盘中的证据和机制; 3）母体循环中的氧化应激标志物;（4）母体血脂异常在氧化应激产生中的潜在作用。一个反复出现的主题是，自由基反应，促进病变胎盘和母体血脂异常之间的“串扰”，促进恶性循环的事件，使因果难以区分，但可能有助于先兆子痫的进展。
The etiology and pathogenesis of the pregnancy syndrome preeclampsia remain poorly understood. There is substantial evidence to suggest that the diverse manifestations of preeclampsia, including altered vascular reactivity, vasospasm, and discrete pathology in many organ systems, are derived from pathologic changes within the maternal vascular endothelium. With the theme of endothelial cell dysfunction emphasized, this review focuses on the role of oxidative stress tan imbalance favoring oxidant over antioxidant forces) in the pathogenesis of preeclampsia, Data are summarized regarding 1) the role of the placenta In preeclampsia; 2) evidence and mechanisms of oxidative stress in the preeclampsia placenta; 3) markers of oxidative stress in the maternal circulation; and 4) the potential role of maternal dyslipidemia in generation of oxidative stress. A recurrent theme is that free radical reactions, promoted by "cross-talk" between the diseased placenta and maternal dyslipidemia, promote a vicious cycle of events that make cause and effect difficult to distinguish but likely contribute to the progression of preeclampsia.