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ABSTRACT
Background
Preeclampsia is a pregnancy-specific hypertensive disorder characterized by the onset of hypertension and proteinuria after the 20th week of gestation in previously normotensive women. It remains a leading cause of maternal and fetal morbidity and mortality worldwide. Delivery of the placenta is currently the only definitive treatment, underscoring its central role in disease pathogenesis.
Objective
This review aims to summarize and integrate current knowledge on the molecular mechanisms underlying the development of preeclampsia, with a focus on placental dysfunction and maternal vascular responses.
Methods
A narrative review of the literature was conducted, focusing on studies investigating the molecular and cellular basis of preeclampsia, including angiogenic imbalance, oxidative stress, inflammation, and dysregulation of vascular signaling pathways.
Results
Placental ischemia, resulting from inadequate trophoblast invasion and insufficient remodeling of maternal spiral arteries, is recognized as a key initiating factor. This leads to reduced uteroplacental perfusion and hypoxia. In response, the ischemic placenta releases a range of bioactive factors into the maternal circulation that promote systemic endothelial dysfunction. These factors contribute to oxidative stress, activation of inflammatory pathways, dysregulation of the renin–angiotensin system, and an imbalance between pro-angiogenic and anti-angiogenic mediators. Collectively, these alterations impair endothelial function, disrupt vascular homeostasis, and result in hypertension and end-organ damage.
Conclusion
Preeclampsia arises from complex and interconnected molecular mechanisms involving placental dysfunction and maternal endothelial injury. A deeper understanding of these pathways may facilitate the identification of novel biomarkers and therapeutic targets, ultimately improving the prevention and management of this disorder.
Keywords: Preeclampsia; Placental ischemia; Endothelial dysfunction; Oxidative stress; Angiogenic imbalance; Inflammation; Renin–angiotensin system