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Updated: Jul 10, 2026

Disruption of the Mouse Blood-Brain Barrier by Small Extracellular Vesicles from Hypoxic Human Placentas
Published on: January 26, 2024
[Preeclampsia as a maternal vascular disease]
Alaa Amash1, Mahmoud Huleihel, Eyal Sheiner
1Department of Microbiology and Immunology, Soroka University Medical Center, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheba, Israel.
Preeclampsia, a pregnancy complication affecting 5-7% of pregnancies, involves placental dysfunction. This review explores the placenta's role and angiogenic factors in preeclampsia development and its impact on maternal and perinatal mortality.
Area of Science:
- Obstetrics and Gynecology
- Maternal-Fetal Medicine
- Pathophysiology
Context:
- Preeclampsia is a significant pregnancy complication impacting 5-7% of pregnancies globally.
- It represents a leading cause of maternal and perinatal mortality worldwide.
- The placenta, specifically trophoblast cells, is central to preeclampsia's development.
Purpose:
- To review current understanding of the placenta's role in preeclampsia pathogenesis.
- To summarize the involvement of angiogenic factors in the disease process.
- To elucidate the two-stage model of preeclampsia development.
Summary:
- Preeclampsia is characterized by two stages: initial defective placentation leading to ischemia/hypoxia, followed by the release of factors causing maternal endothelial and vascular dysfunction.
- Placental ischemia triggers the release of factors into maternal circulation, initiating a cascade of events.
- This cascade results in clinical symptoms like hypertension, proteinuria, and impaired organ function.
Impact:
- Highlights the critical role of placental health in preventing pregnancy complications.
- Provides insights into the molecular mechanisms underlying preeclampsia.
- Informs potential therapeutic strategies targeting placental and angiogenic factors.
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