Abstract
Preeclampsia is a hypertensive pregnancy disorder characterized by development of hypertension and proteinuria after 20 weeks of gestation that remains a leading cause of maternal and neonatal morbidity and mortality. While preeclampsia is believed to result from complex interactions between maternal and placental factors, the proximate pathophysiology of this syndrome remains elusive. Cell-to-cell communication is a critical signaling mechanism for feto-placental development in normal pregnancies. One mechanism of cellular communication relates to activated cell-derived sealed membrane vesicles called extracellular vesicles (EVs). The concentrations and contents of EVs in biological fluids depend upon their cells of origin and the stimuli which trigger their production. Research on EVs in preeclampsia has focused on EVs derived from the maternal vasculature (endothelium, vascular smooth muscle) and blood (erythrocytes, leukocytes, and platelets), as well as placental syncytiotrophoblasts. Changes in the concentrations and contents of these EVs may contribute to the pathophysiology of preeclampsia by accentuating the pro-inflammatory and pro-coagulatory states of pregnancy. This review focuses on possible interactions among placental- and maternal-derived EVs and their contents in the initiation and progression of the pathogenesis of preeclampsia. Understanding the contributions of EVs in the pathogenesis of preeclampsia may facilitate their use as diagnostic and prognostic biomarkers.
Highlights
This article is part of the Topical Collection on PreeclampsiaPreeclampsia is characterized by new-onset hypertension, with either proteinuria (≥300 mg/24 h) and/or organ dysfunction after 20 weeks of gestation [1]
In women for whom extracellular vesicles (EVs) derived from the placenta are the major contributors, we propose that the symptoms of preeclampsia may appear earlier in gestation
Studies examining EVs in non-pregnant women suggest that risk factors for preeclampsia are associated with changes in EVs derived from vascular endothelial cells, leukocytes, and platelets [17,18,19,20,21,22,23,24,25,26] (Table 2)
Summary
Preeclampsia is characterized by new-onset hypertension (systolic blood pressure ≥140 mmHg/diastolic blood pressure ≥90 mmHg), with either proteinuria (≥300 mg/24 h) and/or organ dysfunction after 20 weeks of gestation [1]. There are no established early diagnostic tests or effective targeted pharmacological treatments for preeclampsia. It is recognized increasingly that preeclampsia is a heterogeneous disease, caused by several distinct underlying mechanisms that may result in different clinical phenotypes [5]. This is reflected in current clinical practice, as it is common to divide preeclampsia into early (34 weeks of gestation) preeclampsia based on the
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