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Endothelial Susceptibility-Related Genetic Variants and Hypertensive Disorders of Pregnancy-Brief Report

Linke Li1,2, Yu Zhang3, Buu Truong2

  • 1Center for Genomic Medicine, Massachusetts General Hospital, Boston (L.L., Z.Y., H.T., P.N., M.C.H.).

Arteriosclerosis, Thrombosis, and Vascular Biology
|June 4, 2026
PubMed

Insights

Genetic risk variants for coronary artery disease (CAD) acting on endothelial cells (ECs) are associated with hypertensive disorders of pregnancy (HDPs). This suggests a shared genetic basis for HDPs and CAD, linked by endothelial dysfunction.

Area of Science:

  • Cardiovascular Genetics
  • Reproductive Medicine
  • Genomics

Background:

  • Hypertensive disorders of pregnancy (HDPs), including preeclampsia and gestational hypertension, involve endothelial dysfunction.
  • HDPs share epidemiological and genetic links with coronary artery disease (CAD).
  • Endothelial cell (EC)-acting CAD genetic risk variants may predict treatment response in CAD.

Purpose of the Study:

  • To investigate the association between EC-acting CAD genetic risk variants and HDPs.
  • To determine if a polygenic risk score (PRS) for EC-acting CAD variants is linked to HDP risk.
  • To explore the shared genetic architecture between HDPs and CAD via endothelial dysfunction.

Main Methods:

  • Examined 35 EC-acting and 205 non-EC-acting CAD risk variants.
  • Calculated PRS using EC-acting or non-EC-acting CAD variants in the nuMoM2b cohort.
  • Utilized logistic regression and 2-sample Mendelian randomization to test associations with HDPs, preeclampsia, and gestational hypertension.

Main Results:

  • Higher EC-acting PRS was associated with increased HDP incidence (OR 1.09 per SD, P=0.008).
  • Non-EC-acting PRS showed no significant association with HDP risk (OR 1.05, P=0.14).
  • EC-acting CAD variants were strongly associated with preeclampsia (OR 1.55) and gestational hypertension (OR 1.54) in Mendelian randomization.

Conclusions:

  • PRS and Mendelian randomization analyses indicate an enrichment of EC-acting CAD genetic risk variants in women with HDPs.
  • Findings support a shared genetic architecture between HDPs and CAD.
  • Endothelial dysfunction is a key factor in the shared genetic basis of HDPs and CAD.
Abstract

Keywords:
cardiovascular diseasecoronary artery diseaseendothelial cellgenetic risk scorepregnancy

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