Abstract
The normal maternal cardiovascular adaptation to pregnancy involves a complex physiologic response to the growing conceptus, including alterations in maternal vascular endothelial cells that contribute to a profound fall in total systemic vascular resistance. There is a large body of evidence that adverse changes in the vascular endothelium underlie the multisystemic maternal manifestations of the hypertensive pregnancy disorder preeclampsia. Our knowledge is incomplete regarding the mechanisms of adaptive endothelial changes of normal pregnancy, and why these changes are attenuated or fail in women who develop preeclampsia. Endothelial progenitor cells (EPCs) are a heterogeneous population of cells that exist in both the fetus and adult. These cells can be mobilized into the circulation by growth factors and can then support the health of the vascular endothelium by several mechanisms. This review highlights some of the current understanding of EPCs, their potential role in pregnancy, and emerging evidence for EPC dysfunction in preeclampsia. We speculate that interference with nitric oxide (NO)-driven mobilization or activity of EPCs in the maternal circulation partially contributes to the widespread endothelial dysfunction underlying the clinical manifestations of preeclampsia. Potential roles of EPCs in the placenta and fetus are also considered. © 2010 International Society for the Study of Hypertension in Pregnancy. Published by Elsevier B.V. All rights reserved.
Original language | English |
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Pages (from-to) | 48-58 |
Number of pages | 10 |
Journal | Pregnancy Hypertension |
Volume | 1 |
Issue number | 1 |
DOIs | |
Publication status | Published - Jan 2011 |
Keywords
- Endothelial cells
- Endothelial progenitor cells
- Preeclampsia
- Pregnancy