Mitochondrial Dysfunction in the Pathogenesis of Preeclampsia

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. 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.

Automated summary

Preeclampsia is a common complication in pregnancy, associated with high rates of maternal and perinatal mortality and morbidity. Mitochondrial abnormality is a major contributor to placental dysfunction, which is believed to be the cause of preeclampsia. Circulating bioactive factors released from the placenta can cause mitochondrial damage, leading to endothelial dysfunction and elevated maternal blood pressure.