Mitochondrial Dysfunction in the Pathogenesis of Preeclampsia.

Mitochondrial Dysfunction in the Pathogenesis of Preeclampsia.
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先兆子痫的发病机理中的线粒体功能障碍。

DOI:
10.1007/s11906-022-01184-7
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发表时间:
2022-06
影响因子:
5.6
通讯作者:
--
中科院分区:
医学2区
文献类型:
--
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先兆子痫使 5-10% 的妊娠变得复杂,并且是孕产妇和围产期死亡率和发病率的主要原因。胎盘通过为胎儿提供氧气和营养以及合成激素,在决定妊娠结局方面发挥着关键作用。胎盘功能高度依赖于线粒体提供的能量。众所周知,先兆子痫起源于胎盘功能障碍,但其病因仍不清楚。在过去的三十年中,大量证据表明线粒体异常是胎盘功能障碍的主要原因。此外,胎盘释放的循环生物活性因子引起的线粒体损伤可能会导致内皮功能障碍,进而导致母体血压升高。在这篇综述中,我们总结了目前关于子痫前期发病机制中线粒体异常的知识,并讨论了针对线粒体的子痫前期治疗方法。
Preeclampsia complicates 5–10% of all pregnancies and is a leading cause of maternal and perinatal mortality and morbidity. The placenta plays a pivotal role in determining pregnancy outcome by supplying the fetus with oxygen and nutrients and by synthesizing hormones. Placental function is highly dependent on energy supplied by mitochondria. It is well-known that preeclampsia is originated from placental dysfunction, although the etiology of it remains elusive. During the last three decades, substantial evidence suggests that mitochondrial abnormality is a major contributor to placental dysfunction. In addition, mitochondrial damage caused by circulating bioactive factors released from the placenta may cause endothelial dysfunction and subsequent elevation in maternal blood pressure. In this review, we summarize the current knowledge of mitochondrial abnormality in the pathogenesis of preeclampsia and discuss therapeutic approaches targeting mitochondria for treatment of preeclampsia.
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