Defective Trophoblast Differentiation, Endothelial Dysfunction, and Immune Dysregulation in Preeclampsia Coalesce on a Placental VGLL3-Centered Gene Network
Authors' conclusion
These findings position VGLL3 as a promising novel therapeutic target for preeclampsia.
Study context
- Population
- Preeclamptic placentas (human), mouse and human placental models
Methodological detailshuman single-cell and spatial analyses, in vitro, in vivo and ex vivo models
- Human single-cell and spatial analyses
- In vitro, in vivo and ex vivo models
Main finding
As reported in the abstract
- VGLL3 upregulated in preeclamptic placentas
- VGLL3 promotes immune activation, impairs trophoblast differentiation and induces endothelial dysfunction, contributing to pregnancy-related hypertension, fetal growth restriction and offspring mortality
- VGLL3 acts upstream of preeclampsia-associated processes, incl. sFLT1 production
- Targeting VGLL3 (genetic deletion in mouse placentas or therapeutic inhibition in human placentas) protects against preeclampsia and alleviates disease pathology
Original publication
Defective Trophoblast Differentiation, Endothelial Dysfunction, and Immune Dysregulation in Preeclampsia Coalesce on a Placental VGLL3-Centered Gene Network. Circulation. Published 9 April 2026. doi:10.
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