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Vascular Dysfunction in Preeclampsia. Cells 2021 11 06;10(11)

Date

11/28/2021

Pubmed ID

34831277

Pubmed Central ID

PMC8616535

DOI

10.3390/cells10113055

Scopus ID

2-s2.0-85118544786   12 Citations

Abstract

Preeclampsia is a life-threatening pregnancy-associated cardiovascular disorder characterized by hypertension and proteinuria at 20 weeks of gestation. Though its exact underlying cause is not precisely defined and likely heterogenous, a plethora of research indicates that in some women with preeclampsia, both maternal and placental vascular dysfunction plays a role in the pathogenesis and can persist into the postpartum period. Potential abnormalities include impaired placentation, incomplete spiral artery remodeling, and endothelial damage, which are further propagated by immune factors, mitochondrial stress, and an imbalance of pro- and antiangiogenic substances. While the field has progressed, current gaps in knowledge include detailed initial molecular mechanisms and effective treatment options. Newfound evidence indicates that vasopressin is an early mediator and biomarker of the disorder, and promising future therapeutic avenues include mitigating mitochondrial dysfunction, excess oxidative stress, and the resulting inflammatory state. In this review, we provide a detailed overview of vascular defects present during preeclampsia and connect well-established notions to newer discoveries at the molecular, cellular, and whole-organism levels.

Author List

Opichka MA, Rappelt MW, Gutterman DD, Grobe JL, McIntosh JJ

Authors

Justin L. Grobe PhD Associate Professor in the Physiology department at Medical College of Wisconsin
Jennifer Jury Mcintosh DO Associate Professor in the Obstetrics and Gynecology department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Animals
Blood Vessels
DNA, Mitochondrial
Endothelium, Vascular
Female
Humans
Oxidative Stress
Pre-Eclampsia
Pregnancy
Toll-Like Receptor 9