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...
Guardado en:
Autores principales: | , , , , |
---|---|
Formato: | article |
Lenguaje: | EN |
Publicado: |
MDPI AG
2021
|
Materias: | |
Acceso en línea: | https://doaj.org/article/5e72f90fd76043b9b599367b8881060e |
Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
id |
oai:doaj.org-article:5e72f90fd76043b9b599367b8881060e |
---|---|
record_format |
dspace |
spelling |
oai:doaj.org-article:5e72f90fd76043b9b599367b8881060e2021-11-25T17:10:53ZVascular Dysfunction in Preeclampsia10.3390/cells101130552073-4409https://doaj.org/article/5e72f90fd76043b9b599367b8881060e2021-11-01T00:00:00Zhttps://www.mdpi.com/2073-4409/10/11/3055https://doaj.org/toc/2073-4409Preeclampsia 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.Megan A. OpichkaMatthew W. RappeltDavid D. GuttermanJustin L. GrobeJennifer J. McIntoshMDPI AGarticlepreeclampsiapregnancygestationhypertensionvesselblood pressureBiology (General)QH301-705.5ENCells, Vol 10, Iss 3055, p 3055 (2021) |
institution |
DOAJ |
collection |
DOAJ |
language |
EN |
topic |
preeclampsia pregnancy gestation hypertension vessel blood pressure Biology (General) QH301-705.5 |
spellingShingle |
preeclampsia pregnancy gestation hypertension vessel blood pressure Biology (General) QH301-705.5 Megan A. Opichka Matthew W. Rappelt David D. Gutterman Justin L. Grobe Jennifer J. McIntosh Vascular Dysfunction in Preeclampsia |
description |
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. |
format |
article |
author |
Megan A. Opichka Matthew W. Rappelt David D. Gutterman Justin L. Grobe Jennifer J. McIntosh |
author_facet |
Megan A. Opichka Matthew W. Rappelt David D. Gutterman Justin L. Grobe Jennifer J. McIntosh |
author_sort |
Megan A. Opichka |
title |
Vascular Dysfunction in Preeclampsia |
title_short |
Vascular Dysfunction in Preeclampsia |
title_full |
Vascular Dysfunction in Preeclampsia |
title_fullStr |
Vascular Dysfunction in Preeclampsia |
title_full_unstemmed |
Vascular Dysfunction in Preeclampsia |
title_sort |
vascular dysfunction in preeclampsia |
publisher |
MDPI AG |
publishDate |
2021 |
url |
https://doaj.org/article/5e72f90fd76043b9b599367b8881060e |
work_keys_str_mv |
AT meganaopichka vasculardysfunctioninpreeclampsia AT matthewwrappelt vasculardysfunctioninpreeclampsia AT daviddgutterman vasculardysfunctioninpreeclampsia AT justinlgrobe vasculardysfunctioninpreeclampsia AT jenniferjmcintosh vasculardysfunctioninpreeclampsia |
_version_ |
1718412653027655680 |