Hypoxia and Mitochondrial Dysfunction in Pregnancy Complications
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 metaboli...
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doaj-8257a87bb371496897223c53b03cb2b52021-03-09T00:04:48ZengMDPI AGAntioxidants2076-39212021-03-011040540510.3390/antiox10030405Hypoxia and Mitochondrial Dysfunction in Pregnancy ComplicationsXiang-Qun Hu0Lubo Zhang1Lawrence D. Longo, MD Center for Perinatal Biology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA 92350, USALawrence D. Longo, MD Center for Perinatal Biology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA 92350, USAHypoxia 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.https://www.mdpi.com/2076-3921/10/3/405preeclampsiafetal growth restrictionplacentamitochondriareactive oxygen speciesoxidative stress |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Xiang-Qun Hu Lubo Zhang |
spellingShingle |
Xiang-Qun Hu Lubo Zhang Hypoxia and Mitochondrial Dysfunction in Pregnancy Complications Antioxidants preeclampsia fetal growth restriction placenta mitochondria reactive oxygen species oxidative stress |
author_facet |
Xiang-Qun Hu Lubo Zhang |
author_sort |
Xiang-Qun Hu |
title |
Hypoxia and Mitochondrial Dysfunction in Pregnancy Complications |
title_short |
Hypoxia and Mitochondrial Dysfunction in Pregnancy Complications |
title_full |
Hypoxia and Mitochondrial Dysfunction in Pregnancy Complications |
title_fullStr |
Hypoxia and Mitochondrial Dysfunction in Pregnancy Complications |
title_full_unstemmed |
Hypoxia and Mitochondrial Dysfunction in Pregnancy Complications |
title_sort |
hypoxia and mitochondrial dysfunction in pregnancy complications |
publisher |
MDPI AG |
series |
Antioxidants |
issn |
2076-3921 |
publishDate |
2021-03-01 |
description |
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. |
topic |
preeclampsia fetal growth restriction placenta mitochondria reactive oxygen species oxidative stress |
url |
https://www.mdpi.com/2076-3921/10/3/405 |
work_keys_str_mv |
AT xiangqunhu hypoxiaandmitochondrialdysfunctioninpregnancycomplications AT lubozhang hypoxiaandmitochondrialdysfunctioninpregnancycomplications |
_version_ |
1724228360678146048 |