Endothelial dysfunction: role in the maternal syndrome of preeclampsia and long-term consequences for the cardiovascular system
Preeclampsia is a pregnancy disorder being a leading cause of maternal and fetal mortality and morbidity. It is a complex multisystem disease characterized by hypertension and proteinuria. In preeclampsia the placenta releases factors into the maternal circulation which cause a systemic endothelial...
Saved in:
Published in | Annales de cardiologie et d'angeiologie Vol. 62; no. 3; p. 215 |
---|---|
Main Authors | , , , |
Format | Journal Article |
Language | French |
Published |
France
01.06.2013
|
Subjects | |
Online Access | Get more information |
Cover
Loading…
Summary: | Preeclampsia is a pregnancy disorder being a leading cause of maternal and fetal mortality and morbidity. It is a complex multisystem disease characterized by hypertension and proteinuria. In preeclampsia the placenta releases factors into the maternal circulation which cause a systemic endothelial dysfunction. Here, we review data demonstrating the central role played by the endothelium in the development of the maternal syndrome of preeclampsia. We present also original data showing how circulating factors present in the plasma of preeclamptic women can alter the transcriptome of endothelial cells. The expression of genes involved in essential functions such as vasoregulation, oxidative stress, apoptosis and cell proliferation show differential expression when endothelial cells are exposed to preeclamptic or normal pregnancy plasma. We conclude by discussing the growing evidences that the alterations of the endothelium during preeclampsia are linked to an increased risk of cardiovascular diseases latter on life. Therefore, a better understanding of the modifications undergone by the endothelial cells during preeclampsia is essential to develop new therapeutic approaches to both, manage preeclampsia and to prevent the long-term sequelae of the disease on women cardiovascular system. |
---|---|
ISSN: | 1768-3181 |
DOI: | 10.1016/j.ancard.2013.03.002 |