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Mitochondrial Dysfunction in the Pathogenesis of Preeclampsia

  • Preeclampsia (VD Garovic and AG Kattah, Section Editors)
  • Published:
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Abstract

Purpose of Review

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.

Recent Findings

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.

Summary

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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Fig. 1
Fig. 2

source of cellular reactive oxygen species (ROS). Leakage of electrons at complexes I and III from the ETC leads to partial reduction of oxygen to form superoxide (O2•−). O2•− is rapidly converted to hydrogen peroxide (H2O2) by superoxide dismutases (SODs), which is then reduced to water by glutathione peroxidases (GPXs) and peroxiredoxins (PRXs). The production of ROS at complexes I and III are increased in hypoxic conditions

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Funding

This work was funded by the National Institutes of Health Grants HD083132 (LZ), HL128209 (LZ), HL137649 (LZ) and HL149608 (LZ).

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Correspondence to Xiang-Qun Hu or Lubo Zhang.

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Hu, XQ., Zhang, L. Mitochondrial Dysfunction in the Pathogenesis of Preeclampsia. Curr Hypertens Rep 24, 157–172 (2022). https://doi.org/10.1007/s11906-022-01184-7

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