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Placental mitochondria and reactive oxygen species in the physiology and pathophysiology of pregnancy
Author(s) -
Fisher Joshua J.,
Bartho Lucy A.,
Perkins Anthony V.,
Holland Olivia J.
Publication year - 2020
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.13172
Subject(s) - syncytiotrophoblast , mitochondrion , placenta , reactive oxygen species , pregnancy , preeclampsia , biology , gestational diabetes , microbiology and biotechnology , fetus , gestation , genetics
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.