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Related Experiment Video

Updated: Jun 10, 2026

Disruption of the Mouse Blood-Brain Barrier by Small Extracellular Vesicles from Hypoxic Human Placentas

Disruption of the Mouse Blood-Brain Barrier by Small Extracellular Vesicles from Hypoxic Human Placentas

Published on: January 26, 2024

New markers in preeclampsia.

Alexandre Hertig¹, Philippe Liere

¹Inserm U702, Hôpital Tenon, Paris, France. alexandre.hertig@tnn.aphp.fr

Clinica Chimica Acta; International Journal of Clinical Chemistry

|July 28, 2010

Summary

This summary is machine-generated.

Preeclampsia (PE) is a common pregnancy complication. Biomarkers like sFlt1 and sEng show promise for early detection, aiding risk identification before clinical symptoms appear.

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Last Updated: Jun 10, 2026

Disruption of the Mouse Blood-Brain Barrier by Small Extracellular Vesicles from Hypoxic Human Placentas

Disruption of the Mouse Blood-Brain Barrier by Small Extracellular Vesicles from Hypoxic Human Placentas

Published on: January 26, 2024

Area of Science:

Obstetrics and Gynecology
Maternal-Fetal Medicine
Biomarker Discovery

Background:

Preeclampsia (PE) complicates approximately 5% of pregnancies globally.
Despite its prevalence, effective treatments remain elusive, though risk identification has improved.
Elevated levels of soluble Fms-like tyrosine kinase-1 (sFlt1) and soluble endoglin (sEng) precede clinical PE symptoms.

Purpose of the Study:

To review and compare the clinical utility of emerging biomarkers for preeclampsia.
To discuss the pathophysiological roles of sFlt1, sEng, and other potential pathways in PE.
To evaluate the potential for new diagnostic and therapeutic strategies for PE.

Main Methods:

Literature review of current research on preeclampsia biomarkers.
Analysis of the role of sFlt1, sEng, placental growth factor (PlGF), and vascular endothelial growth factor (VEGF) in PE.
Exploration of potential roles for placental steroidogenesis and angiotensin receptor tolerance in PE pathogenesis.

Main Results:

sFlt1 and sEng are significantly elevated in maternal blood weeks before PE onset.
A decrease in VEGF and PlGF is concurrently observed in women with PE.
Defective placental steroidogenesis and altered angiotensin receptor tolerance are implicated in mouse models of PE.

Conclusions:

sFlt1 and sEng are highly promising biomarkers for early preeclampsia detection.
Further research is needed to elucidate the role of these biomarkers and pathways in human PE.
Investigating these pathways may lead to novel therapeutic interventions for preeclampsia.