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Endothelial function and circulating biomarkers are disturbed in women and children after preeclampsia
Anne Stine Kvehaugen1, Ralf Dechend, Heidi Bente Ramstad
1Department of Obstetrics and Gynecology, Oslo University Hospital, Ulleval, Oslo, Norway.
Insights
Preeclampsia in mothers, especially with small for gestational age infants, leads to lasting endothelial dysfunction in both mother and child, increasing cardiovascular risk across generations.
Area of Science:
- Cardiovascular disease
- Maternal-fetal medicine
- Endocrinology
Background:
- Preeclampsia is a significant risk factor for long-term maternal cardiovascular disease.
- Shared pathophysiological pathways, including endothelial dysfunction, link preeclampsia and cardiovascular diseases.
- The transgenerational impact of preeclampsia on offspring cardiovascular health remains an area of investigation.
Purpose of the Study:
- To investigate endothelial function and circulating biomarkers in mother-child pairs years after preeclampsia.
- To determine if maternal biomarkers at delivery predict long-term postpartum findings.
- To assess the impact of early-onset preeclampsia and small for gestational age (SGA) infants.
Main Methods:
- Longitudinal study comparing 26 mother-child pairs post-preeclampsia with 17 control pairs 5-8 years postpartum.
- Noninvasive assessment of endothelial function.
- Measurement of maternal circulating biomarkers (lipid metabolism, angiogenesis, inflammation).
Main Results:
- Reduced endothelial function observed in both mothers and children following preeclampsia with SGA infants.
- Elevated postpartum maternal soluble fms-like tyrosine kinase 1 and high-sensitivity C-reactive protein in the preeclampsia group.
- Increased frequency of high maternal biomarker concentrations at delivery and postpartum in the preeclampsia group.
Conclusions:
- Preeclampsia, particularly with SGA infants, results in persistent endothelial dysfunction in both mothers and children.
- Elevated inflammatory and antiangiogenic maternal biomarkers are associated with preeclampsia and its long-term effects.
- Findings support the concept of transgenerational cardiovascular risk transmission following preeclamptic pregnancies.
Abstract:
Preeclampsia is a long-term cardiovascular risk factor for the mother and possibly the offspring. Preeclampsia and cardiovascular diseases share common pathophysiological features, including endothelial dysfunction. We explored whether endothelial function, measured noninvasively, as well as circulating biomarkers reflecting lipid metabolism, angiogenesis, and inflammation, differed in paired mothers and offspring 5 to 8 years after delivery. Twenty-six mother and child pairs after pregnancies complicated by preeclampsia were compared with 17 mother and child pairs after uncomplicated pregnancies. In addition, we assessed whether concentrations of maternal circulating biomarkers at delivery predicted findings 5 to 8 years postpartum. We also included an assessment of early onset preeclampsia and specifically addressed the effects of small for gestational age. Endothelial function was significantly reduced in both mothers and children after preeclampsia when combined with a small-for-gestational-age infant compared with mothers and children after pregnancies without a small-for-gestational-age infant (mothers: P<0.001; children: P<0.05). Postpartum maternal soluble fms-like tyrosine kinase 1 (P=0.05) and high-sensitivity C-reactive protein (P=0.02) were elevated in the preeclampsia group compared with controls. High concentrations of these maternal biomarkers both at delivery and 5 to 8 years postpartum were also more frequent in preeclampsia compared with controls (P<0.05). The novelty of our study is the parallel finding of reduced endothelial function in mother and child pairs 5 to 8 years after small-for-gestational-age preeclamptic pregnancies, accompanied by increased inflammatory and antiangiogenic maternal biomarkers. This finding supports the concept of transgenerational risk of cardiovascular disease after preeclampsia.
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