Related Experiment Video
Updated: Jun 27, 2026
Disruption of the Mouse Blood-Brain Barrier by Small Extracellular Vesicles from Hypoxic Human Placentas
Published on: January 26, 2024
Angiogenic factors and pre-eclampsia: an early marker is needed
1Department of Obstetrics, Leipzig University, Liebigstr. 20a, 04103 Leipzig, Germany. holger.stepan@medizin.uni-leipzig.de
Insights
A new study suggests VEGF(165)b, a protein variant, is elevated in normal pregnancies but decreased in pre-eclampsia. This finding could lead to better early detection of pre-eclampsia.
Area of Science:
- Reproductive medicine
- Maternal-fetal medicine
- Molecular biology
Background:
- Pre-eclampsia is a leading cause of maternal and neonatal mortality and morbidity.
- Imbalances in angiogenic factors (e.g., vascular endothelial growth factor [VEGF]) and anti-angiogenic factors (e.g., soluble fms-like tyrosine kinase 1 [sFlt1]) are implicated in pre-eclampsia pathogenesis.
- Current diagnostic and prognostic markers for pre-eclampsia are limited.
Discussion:
- Bills and colleagues identified VEGF(165)b, an alternative splice variant of VEGF pre-mRNA.
- VEGF(165)b levels were found to be upregulated in normal pregnancies.
- In women who developed pre-eclampsia, the upregulation of VEGF(165)b was delayed or diminished.
Key Insights:
- VEGF(165)b shows differential expression patterns between normal pregnancy and pre-eclampsia.
- This protein variant may play a role in the angiogenic balance during pregnancy.
- The altered expression of VEGF(165)b suggests its potential as a biomarker for pre-eclampsia.
Outlook:
- VEGF(165)b could serve as a novel marker for pre-eclampsia risk assessment, potentially in combination with other parameters.
- Further research is warranted to validate VEGF(165)b as a clinical biomarker for early pre-eclampsia detection and management.
- Understanding the precise role of VEGF(165)b in pregnancy physiology and pathophysiology may reveal new therapeutic targets.
Abstract:
Pre-eclampsia, a pregnancy complication characterized by hypertension and proteinuria, is still a major cause of neonatal and maternal mortality, and acute and long-term morbidities for both mother and neonate. There is mounting evidence that an imbalance between angiogenic factors, such as VEGF (vascular endothelial growth factor) or PlGF (placental growth factor), and factors inhibiting angiogenesis, such as sFlt1 (soluble fms-like tyrosine kinase 1) and sEng (soluble endoglin), are closely related to the pathogenesis of pre-eclampsia. In the present issue of Clinical Science, Bills and co-workers report that VEGF(165)b, an alternative splice variant of the VEGF pre-mRNA, is up-regulated in women with normal pregnancy and that this increase was delayed or diminished in women who developed pre-eclampsia. Thus this protein could serve (alone or in combination with other parameters) as a new marker for risk assessment in terms of pre-eclampsia.
