Hypoxia and Mitochondrial Dysfunction in Pregnancy Complications.
Hypoxia and Mitochondrial Dysfunction in Pregnancy Complications.
复制标题
妊娠并发症中的缺氧和线粒体功能障碍。
DOI：
10.3390/antiox10030405
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发表时间：
2021-03-08
期刊：
影响因子：
--
通讯作者：
Zhang L
中科院分区：
文献类型：
--
作者：
Hu XQ;Zhang L
低氧是机体内环境平衡机制的常见和严重的应激，妊娠期低氧与先兆子痫的母体并发症发生率显著增加相关，对胎儿发育和随后的心血管和代谢疾病的风险产生不利影响。人类和动物研究表明，子宫血管阻力增加和胎盘低氧在子痫前期和妊娠低氧相关的胎儿/胎儿生长受限(FGR/IUGR)中起致病作用。妊娠低氧对子宫胎盘细胞线粒体产生过多的活性氧(ROS)有重要影响，从而导致氧化应激。过多的线粒体ROS通过破坏细胞大分子进而导致子宫胎盘功能障碍，这是子痫前期和FGR发病的基础。本文就低氧诱导的线粒体ROS及其在胎盘功能障碍和妊娠并发症发病机制中的作用作一综述。此外，还讨论了选择性靶向胎盘细胞线粒体ROS的治疗方法。
Hypoxia is a common and severe stress to an organism’s homeostatic mechanisms, and hypoxia during gestation is associated with significantly increased incidence of maternal complications of preeclampsia, adversely impacting on the fetal development and subsequent risk for cardiovascular and metabolic disease. Human and animal studies have revealed a causative role of increased uterine vascular resistance and placental hypoxia in preeclampsia and fetal/intrauterine growth restriction (FGR/IUGR) associated with gestational hypoxia. Gestational hypoxia has a major effect on mitochondria of uteroplacental cells to overproduce reactive oxygen species (ROS), leading to oxidative stress. Excess mitochondrial ROS in turn cause uteroplacental dysfunction by damaging cellular macromolecules, which underlies the pathogenesis of preeclampsia and FGR. In this article, we review the current understanding of hypoxia-induced mitochondrial ROS and their role in placental dysfunction and the pathogenesis of pregnancy complications. In addition, therapeutic approaches selectively targeting mitochondrial ROS in the placental cells are discussed.
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影响因子：
9.7
作者：
Bastian A;Matsuzaki S;Humphries KM;Pharaoh GA;Doshi A;Zaware N;Gangjee A;Ihnat MA
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DOI：
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发表时间：
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影响因子：
2.8
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