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Associations of Genetically Predicted NPR3 and NPR2 Perturbation and Preeclampsia Risk: A Two-Sample Mendelian

Roxane de La Harpe1, Tormod Rogne2,3, Michael Nyberg4

  • 1Department of Medicine, University Hospital of Lausanne, Lausanne, Vaud, Switzerland.

International Journal of Hypertension
|May 23, 2025
PubMed
Summary

C-type natriuretic peptide (CNP) may reduce preeclampsia risk by affecting NPR3 function. Genetic analysis suggests reduced NPR3 function is linked to lower preeclampsia incidence, offering potential therapeutic insights.

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Area of Science:

  • Obstetrics and Gynecology
  • Cardiovascular Research
  • Genetics and Genomics

Background:

  • Preeclampsia is a pregnancy complication characterized by hypertension after 20 weeks of gestation, stemming from placental factors that impair maternal vascular function.
  • C-type natriuretic peptide (CNP) possesses vasodilatory properties and may counteract preeclampsia-related vascular dysfunction.

Purpose of the Study:

  • To investigate the potential effect of C-type natriuretic peptide (CNP) on preeclampsia risk using a Mendelian randomization (MR) framework.
  • To explore the association between genetic variants related to CNP signaling pathways (NPR2 activation and NPR3 clearance) and preeclampsia risk.

Main Methods:

  • Utilized genetic instrumental variables from a large-scale, multiancestry genome-wide association study (GWAS) involving over 5 million individuals.
  • Conducted two-sample MR analyses using female-specific data from the UK Biobank (198,402 participants) and the largest available GWAS on preeclampsia (296,824 participants).
  • Assessed the impact of genetically proxied NPR2 activation and NPR3 function on preeclampsia risk, with sensitivity analyses to evaluate pleiotropy.

Main Results:

  • Genetically proxied reduced NPR3 function was significantly associated with a lower risk of preeclampsia (OR: 0.46, 95% CI 0.30-0.69).
  • Genetically proxied increased NPR2 activation showed no significant association with preeclampsia risk, potentially due to underpowered genetic instruments.
  • Sensitivity analyses confirmed robust findings with minimal evidence of pleiotropy, supporting the targeted biological pathways.

Conclusions:

  • The MR study provides genetic evidence that reduced NPR3 function, a pathway influenced by CNP, is associated with a protective effect against preeclampsia risk.
  • Further research and evidence are needed before clinical development can be pursued to explore CNP as a potential preeclampsia treatment.