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Published on: January 26, 2024
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Genetic Variants Associated With Preeclampsia and Maternal Serum sFLT1 Levels
Jasmine A Mack1,2, Ulla Sovio1,3, Felix R Day4
1Department of Obstetrics and Gynaecology, School of Clinical Medicine (J.A.M., U.S., F.G., E.C., D.S.C.-J., G.C.S.S.), University of Cambridge, United Kingdom.
Hypertension (Dallas, Tex. : 1979)
|December 26, 2024
Summary
Maternal and fetal genomes influence soluble fms-like tyrosine kinase 1 (sFLT1) levels in preeclampsia. Fetal genes impact late-pregnancy sFLT1, while maternal genes may offer early protection against preeclampsia.
Area of Science:
- Obstetrics and Gynecology
- Genetics
- Perinatology
Background:
- Elevated maternal serum soluble fms-like tyrosine kinase 1 (sFLT1) is crucial in preeclampsia pathophysiology.
- Understanding the genetic influences on sFLT1 levels is key to managing preeclampsia.
Purpose of the Study:
- To investigate the relationship between maternal and fetal genomes and maternal sFLT1 levels.
- To analyze sFLT1 and sFLT1:placental growth factor (PlGF) ratio Z-scores across gestation.
Main Methods:
- Prospective cohort study of 3968 nulliparous mother-child pairs.
- Genomic analysis using prior fetal and maternal genome-wide association studies for preeclampsia.
- Assessed sFLT1 and sFLT1:PlGF Z-scores at 12, 20, 28, and 36 weeks gestational age.
Main Results:
- Fetal genetic variants were associated with sFLT1 and sFLT1:PlGF Z-scores at 36 weeks gestational age.
- FLT1 enhancer SNPs correlated with increased sFLT1 levels in late pregnancy (Δ36-28).
- Maternal polygenic risk scores for preeclampsia were linked to lower first-trimester sFLT1 and a greater rise in third-trimester sFLT1.
Conclusions:
- Findings support a causal role for placental sFLT1 in preeclampsia development.
- Maternal genetic factors may contribute to protective effects in early pregnancy and influence sFLT1 rise in the third trimester.
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