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Trends Mol Med. 2015 Feb;21(2):88-97. doi: 10.1016/j.molmed.2014.11.009. Epub 2014 Dec 2.

Molecular mechanisms of maternal vascular dysfunction in preeclampsia.

Author information

1
Department of Integrative Physiology and Anatomy, University of North Texas Health Science Center, Fort Worth, TX, USA; Department of Obstetrics and Gynecology, University of North Texas Health Science Center, Fort Worth, TX, USA.
2
Department of Obstetrics and Gynecology, University of Alberta, Edmonton, Canada; Department of Physiology, University of Alberta, Edmonton, Canada; Women and Children's Health Research Institute, Edmonton, Canada. Electronic address: sandra.davidge@ualberta.ca.

Abstract

In preeclampsia, as a heterogeneous syndrome, multiple pathways have been proposed for both the causal as well as the perpetuating factors leading to maternal vascular dysfunction. Postulated mechanisms include imbalance in the bioavailability and activity of endothelium-derived contracting and relaxing factors and oxidative stress. Studies have shown that placenta-derived factors [antiangiogenic factors, microparticles (MPs), cell-free nucleic acids] are released into the maternal circulation and act on the vascular wall to modify the secretory capacity of endothelial cells and alter the responsiveness of vascular smooth muscle cells to constricting and relaxing stimuli. These molecules signal their deleterious effects on the maternal vascular wall via pathways that provide the molecular basis for novel and effective therapeutic interventions.

KEYWORDS:

endothelial function; hypertension; preeclampsia; pregnancy

PMID:
25541377
DOI:
10.1016/j.molmed.2014.11.009
[Indexed for MEDLINE]

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