Vascular Dysfunction in Preeclampsia

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 preecla...

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Bibliographic Details
Published in:Cells (Basel, Switzerland) Switzerland), 2021-11, Vol.10 (11), p.3055
Main Authors: Opichka, Megan A, Rappelt, Matthew W, Gutterman, David D, Grobe, Justin L, McIntosh, Jennifer J
Format: Article
Language:English
Subjects:
Animals
blood pressure
Blood Vessels - pathology
Blood Vessels - physiopathology
Diabetes
Disease
DNA, Mitochondrial - metabolism
Eclampsia
Endothelium, Vascular - pathology
Endothelium, Vascular - physiopathology
Female
gestation
Humans
Hypertension
Hypoxia
Inflammation
Kinases
MicroRNAs
Mitochondria
Molecular modelling
Obstetrics
Oxidative Stress
Pathophysiology
Pre-eclampsia
Pre-Eclampsia - pathology
Pre-Eclampsia - physiopathology
Preeclampsia
Pregnancy
Premature birth
Proteinuria
Review
Risk factors
Toll-Like Receptor 9 - metabolism
Uterus
Vasopressin
vessel
Womens health
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Summary: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.
ISSN:2073-4409
2073-4409
DOI:10.3390/cells10113055