Placental mitochondrial impairment in preeclampsia patients

Preeclampsia is a pregnancy-specific hypertensive disorder characterized by new-onset hypertension after 20 weeks of gestation, accompanied by end-organ dysfunction with or without proteinuria. Affecting approximately 5-7% of pregnancies worldwide, it remains a leading cause of maternal and fetal morbidity and mortality. Despite decades of research, the underlying pathophysiology of preeclampsia remains incompletely understood. However, increasing evidence implicates placental mitochondrial oxidative stress in its pathogenesis. In this review, we summarize the current literature pertaining to ultrastructural evidence of mitochondrial damage, defects in oxidative phosphorylation and electron transport chain activity, and alterations in reactive oxygen species production, antioxidant defense, and mitochondrial biogenesis. Finally, we discuss translational considerations and highlight how therapeutic strategies targeted at restoring mitochondrial function may represent a promising approach for managing preeclampsia.