Developmental origins of accelerated cardiovascular aging

¹ Ural State Medical University, Department of Physiology, 620028 Repin str.3, Yekaterinburg, Russia
² Ural Scientific Research Institute of Maternity and Child Care, Department of Biophysics, 620028 Repin str.1, Yekaterinburg, Russia

^* Corresponding author: Pavel.tsyvian@gmail.com

Abstract

The Barker hypothesis of fetal origins of disease, derived from observational epidemiological studies, has been modified by the realization that the early influences on cardiovascular development may be recognized in the fetus. Aging and developmental programming are both associated with oxidative stress and endothelial dysfunction, suggesting common mechanistic origins. Preeclampsia (PE) is the utmost variant of placental insufficiency and is associated with an increase of serum concentrations of inflammation and antiangiogenic agents in mother and fetus. All these factors are specific for the endothelial dysfunction and able to trigger the epigenetic programming of cardiovascular diseases and accelerated aging. The concentrations of cytokines, tumor necrosis factor, C-reactive protein, NO metabolites, endothelin-1 and homocysteine were measured in serum of women with a normal pregnancy (n=27), PE (n=30) and their newborn infants. The concentrations of all these factors were higher in serum of women and newborns of PE group than in serum of women and newborns of the normal group. The significantly positive correlation between factors concentrations in maternal and newborn’s serum was demonstrated in all groups. We suggest the common source of these agents to be the syncytiotrophoblast cells contacting with both maternal and fetal blood and play a significant role in intrauterine programming and epigenetic triggering of accelerated cardiovascular aging.