Placental mitochondria and reactive oxygen species in the physiology and pathophysiology of pregnancy

Mitochondria are central to cell function. The placenta forms the interface between maternal and fetal systems, and placental mitochondria have critical roles in maintaining pregnancy. The placenta is unusual in having two adjacent cell layers (cytotrophoblasts and the syncytiotrophoblast) with vast...

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Bibliographic Details
Published inClinical and experimental pharmacology & physiology Vol. 47; no. 1; pp. 176 - 184
Main Authors Fisher, Joshua J., Bartho, Lucy A., Perkins, Anthony V., Holland, Olivia J.
Format Journal Article
LanguageEnglish
Published Australia Wiley Subscription Services, Inc 01.01.2020
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Summary:Mitochondria are central to cell function. The placenta forms the interface between maternal and fetal systems, and placental mitochondria have critical roles in maintaining pregnancy. The placenta is unusual in having two adjacent cell layers (cytotrophoblasts and the syncytiotrophoblast) with vastly different mitochondria that have distinct functions in health and disease. Mitochondria both produce the majority of reactive oxygen species (ROS), and are sensitive to ROS. ROS are important in allowing cells to sense their environment through mitochondrial‐centred signalling, and this signalling also helps cells/tissues adapt to changing environments. However, excessive ROS are damaging, and increased ROS levels are associated with pregnancy complications, including the important disorders preeclampsia and gestational diabetes mellitus. Here we review the function of placental mitochondria in healthy pregnancy, and also in pregnancy complications. Placental mitochondria are critical to cell function, and mitochondrial damage is a feature of pregnancy complications. However, the responsiveness of mitochondria to ROS signalling may be central to placental adaptations that mitigate damage, and placental mitochondria are an attractive target for the development of therapeutics to improve pregnancy outcomes.
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ISSN:0305-1870
1440-1681
1440-1681
DOI:10.1111/1440-1681.13172