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Published on: January 26, 2024
Maternal cardiovascular-related single nucleotide polymorphisms, genes, and pathways associated with early-onset
Paula Benny1, Kelly Yamasato2, Breck Yunits1
1University of Hawaii Cancer Center, Honolulu, Hawai'i, United States of America.
Insights
This study identified 68 genes and 23 cardiovascular disease processes linked to early-onset preeclampsia. These findings suggest genetic links between preeclampsia and future cardiovascular disease risk.
Area of Science:
- Genetics
- Cardiovascular Disease
- Obstetrics
Background:
- Preeclampsia, affecting 5% of pregnancies, is a condition causing hypertension and proteinuria with no known cure.
- Women with preeclampsia face increased risks of cardiovascular disease later in life.
- The genetic basis and molecular mechanisms of preeclampsia and its associated maternal cardiovascular risk remain poorly understood, especially across diverse ethnic populations.
Purpose of the Study:
- To identify cardiovascular/metabolic single nucleotide polymorphisms (SNPs), genes, and regulatory pathways associated with early-onset preeclampsia.
- To explore the genetic underpinnings of preeclampsia and its connection to long-term cardiovascular health.
- To address the research gap concerning preeclampsia-associated maternal cardiovascular risk in different ethnic groups.
Main Methods:
- Maternal DNA from 31 early-onset preeclampsia cases and 29 controls were analyzed using the MetaboChip genotyping array (~197,000 SNPs).
- Exclusion criteria included multiple gestations and pre-existing medical conditions predisposing to preeclampsia.
- Statistical analyses involved SNPAssoc for SNP analysis, Truncated Product Method for gene association, and Ingenuity Pathway Analysis for disease processes and regulatory networks.
Main Results:
- No individual SNPs were significantly associated with early-onset preeclampsia after multiple comparison correction.
- Gene-based tests revealed significant associations for 68 genes and 23 cardiovascular disease-related processes.
- Identified gene regulatory networks were involved in cellular movement, cardiovascular disease, and inflammatory disease.
Conclusions:
- Multiple cardiovascular genes and disease pathways are significantly associated with early-onset preeclampsia.
- These findings open new avenues for research into the genetic determinants of early-onset preeclampsia.
- The study highlights potential genetic links between preeclampsia and an increased risk of future cardiovascular disease.
Introduction:
Preeclampsia is a medical condition complicated with hypertension and proteinuria during pregnancy. While preeclampsia affects approximately 5% of pregnancies, it remains without a cure. In addition, women who had preeclampsia during pregnancy have been reported to have an increased risk for cardiovascular disease later in life. However, the disease etiology and molecular mechanisms remain poorly understood. The paucity in the literature on preeclampsia associated maternal cardiovascular risk in different ethnic populations also present a need for more research. Therefore, the objective of this study was to identify cardiovascular/metabolic single nucleotide polymorphisms (SNPs), genes, and regulatory pathways associated with early-onset preeclampsia.
Materials And Methods:
We compared maternal DNAs from 31 women with early-onset preeclampsia with those from a control group of 29 women without preeclampsia who delivered full-term normal birthweight infants. Women with multiple gestations and/or known medical disorders associated with preeclampsia (pregestational diabetes, chronic hypertension, renal disease, hyperthyroidism, and lupus) were excluded. The MetaboChip genotyping array with approximately 197,000 SNPs associated with metabolic and cardiovascular traits was used. Single nucleotide polymorphism analysis was performed using the SNPAssoc program in R. The Truncated Product Method was used to identify significantly associated genes. Ingenuity Pathway Analysis and Ingenuity Causal Network Analysis were used to identify significantly associated disease processes and regulatory gene networks respectively.
Results:
The early-onset preeclampsia group included 45% Filipino, 26% White, 16% other Asian, and 13% Native Hawaiian and other Pacific Islanders, which did not differ from the control group. There were no SNPs associated with early-onset preeclampsia after correction for multiple comparisons. However, through gene-based tests, 68 genes and 23 cardiovascular disease-related processes were found to be significantly associated. Associated gene regulatory networks involved cellular movement, cardiovascular disease, and inflammatory disease.
Conclusions:
Multiple cardiovascular genes and diseases demonstrate associations with early-onset preeclampsia. This unfolds new areas of research regarding the genetic determinants of early-onset preeclampsia and their relation to future cardiovascular disease.
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