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Peer-reviewedCC BYCells

Beyond the Biomarkers: Gestation-Dependent Roles of sFLT-1 and PlGF in Human and Non-Human Mammalian Placental Development and Function.

  • Zoe Byrne1,2
  • Sonja Brennan1,2
  • David Watson1,2
  • Donna Rudd2
  • Yoga Kandasamy2,3
  1. 1Maternal Fetal Medicine Unit, Obstetrics & Gynaecology Department, Townsville Hospital and Health Service, 100 Angus Smith Drive, Douglas, Townsville, QLD 4810, Australia.
  2. 2College of Medicine and Dentistry, James Cook University, Townsville, QLD 4810, Australia.
  3. 3Neonatal Intensive Care Unit, Townsville Hospital and Health Service, Townsville, QLD 4810, Australia.
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Abstract

Placental growth factor (PlGF) and soluble fms-like tyrosine kinase-1 (sFLT-1) are established biomarkers of placental dysfunction, but their functions extend beyond the maternal circulating ratio. This structured narrative review examines the FLT1-PlGF-vascular endothelial growth factor system across implantation, trophoblast differentiation, uterine vascular transformation, foetoplacental angiogenesis, exchange capacity development and late-gestational maturation. Human evidence is integrated with selected non-human mammalian studies according to gestational stage, cellular source, anatomical compartment, molecular isoform and placental architecture. We use a compartmentalised angiogenic rheostat as a qualitative organising framework, not an experimentally validated model. It integrates established ligand-receptor biology with human observations and experimental perturbations: PlGF modifies FLT1 signalling and VEGF-A availability, whereas membrane and soluble FLT1 influence ligand distribution and vascular responses. Experimental evidence supports physiological ligand restraint and the pathogenic effects of excessive sFLT-1; human associations do not invariably establish the initiating placental lesion. Pre-eclampsia, foetal growth restriction and invasive placentation illustrate distinct contexts in which angiogenic regulation may become maladaptive. The maternal sFLT-1/PlGF ratio is therefore interpreted as a circulating indicator of placental vascular stress rather than a direct measurement of local signalling.

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Cite

BibTeXRIS
BibTeX
@article{byrne2026beyond,
  title = {{Beyond the Biomarkers: Gestation-Dependent Roles of sFLT-1 and PlGF in Human and Non-Human Mammalian Placental Development and Function.}},
  author = {Zoe Byrne and Sonja Brennan and David Watson and Donna Rudd and Yoga Kandasamy},
  journal = {Cells},
  year = {2026},
  month = oct,
  doi = {10.3390/cells15191817},
  url = {https://europepmc.org/article/MED/42882516},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Beyond the Biomarkers: Gestation-Dependent Roles of sFLT-1 and PlGF in Human and Non-Human Mammalian Placental Development and Function.
AU  - Zoe Byrne
AU  - Sonja Brennan
AU  - David Watson
AU  - Donna Rudd
AU  - Yoga Kandasamy
PY  - 2026
DA  - 2026/10/06
JO  - Cells
DO  - 10.3390/cells15191817
UR  - https://europepmc.org/article/MED/42882516
AB  - Placental growth factor (PlGF) and soluble fms-like tyrosine kinase-1 (sFLT-1) are established biomarkers of placental dysfunction, but their functions extend beyond the maternal circulating ratio. This structured narrative review examines the FLT1-PlGF-vascular endothelial growth factor system across implantation, trophoblast differentiation, uterine vascular transformation, foetoplacental angiogenesis, exchange capacity development and late-gestational maturation. Human evidence is integrated with selected non-human mammalian studies according to gestational stage, cellular source, anatomical compartment, molecular isoform and placental architecture. We use a compartmentalised angiogenic rheostat as a qualitative organising framework, not an experimentally validated model. It integrates established ligand-receptor biology with human observations and experimental perturbations: PlGF modifies FLT1 signalling and VEGF-A availability, whereas membrane and soluble FLT1 influence ligand distribution and vascular responses. Experimental evidence supports physiological ligand restraint and the pathogenic effects of excessive sFLT-1; human associations do not invariably establish the initiating placental lesion. Pre-eclampsia, foetal growth restriction and invasive placentation illustrate distinct contexts in which angiogenic regulation may become maladaptive. The maternal sFLT-1/PlGF ratio is therefore interpreted as a circulating indicator of placental vascular stress rather than a direct measurement of local signalling.
SN  - 2073-4409
ER  -