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Updated: Jan 3, 2026

Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles
Published on: January 26, 2024
[PREECLAMPSIA: PATHOGENESIS AND MECHANISMS BASED THERAPEUTIC APPROACHES]
Zaher Armaly1, Maha Zaher1, Safa Knaneh1
1Department of Nephrology, E.M.M.S. Hospital, Nazareth, and the Galilee Faculty of Medicine-Bar-Ilan University, Zafed, Israel.
Introduction:
Preeclampsia is a serious complication of pregnancy affecting 3-8% of all pregnancies. It increases the morbidity and mortality of both the fetus and the pregnant woman, especially in developing countries. It deleteriously affects several vital organs, including the kidney, heart, liver, brain, and lung. Although, the pathogenesis of preeclampsia has not yet been fully understood, growing evidence suggests that aberrations in the angiogenic factors levels/activity and coagulopathy are responsible for the clinical manifestations of the disease. The common nominator of tissue damage of all these target organs is endothelial injury, which impedes their normal function. At the renal level, glomerular endothelial injury leads to the development of maternal hypertension and proteinuria. Similarly, this disease can cause hepatic and neurologic dysfunction due to vascular damage. The current review summarizes the recent development in the pathogenesis of this disease state with special focus on novel diagnostic biomarkers and their relevance to potential therapeutic options for preeclampsia. Specifically, we will highlight the renal manifestations of the diseases with emphasis on the involvement of angiogenic factors in vascular injury and how restoration of the angiogenic balance affects the renal and cardiovascular outcome of preeclamptic women.
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