The Molecular Basis of the Augmented Cardiovascular Risk in Offspring of Mothers with Hypertensive Disorders of Pregnancy

Abstract

The review examines the impact of maternal preeclampsia (PE) on the cardiometabolic and cardiovascular health of offspring. PE, a hypertensive disorder of pregnancy, is responsible for 2 to 8% of pregnancy-related complications. It significantly contributes to adverse outcomes for their infants, affecting the time of birth, the birth weight, and cardiometabolic risk factors such as blood pressure, body mass index (BMI), abdominal obesity, lipid profiles, glucose, and insulin. Exposure to PE in utero predisposes offspring to an increased risk of cardiometabolic diseases (CMD) and cardiovascular diseases (CVD) through mechanisms that are not fully understood. The incidence of CMD and CVD is constantly increasing, whereas CVD is the main cause of morbidity and mortality globally. A complex interplay of genes, environment, and developmental programming is a plausible explanation for the development of endothelial dysfunction, which leads to atherosclerosis and CVD. The underlying molecular mechanisms are angiogenic imbalance, inflammation, alterations in the renin–angiotensin–aldosterone system (RAAS), endothelium-derived components, serotonin dysregulation, oxidative stress, and activation of both the hypothalamic–pituitary–adrenal axis and hypothalamic–pituitary–gonadal axis. Moreover, the potential role of epigenetic factors, such as DNA methylation and microRNAs as mediators of these effects is emphasized, suggesting avenues for future research and therapeutic interventions.

Keywords

• preeclampsia
• atherosclerosis
• endothelial dysfunction
• cardiometabolic risk factors