Epigenetic processes during preeclampsia and effects on fetal development and chronic health.
Animals
Blood Pressure
/ genetics
Cardiovascular Diseases
/ genetics
Chromatin Assembly and Disassembly
DNA Methylation
Epigenesis, Genetic
Female
Fetal Development
Fetal Growth Retardation
/ genetics
Gene Expression Regulation, Developmental
Humans
Infant, Low Birth Weight
Infant, Newborn
Placenta
/ metabolism
Placentation
/ genetics
Pre-Eclampsia
/ genetics
Pregnancy
Prenatal Exposure Delayed Effects
Prognosis
Risk Assessment
Risk Factors
Epigentics
Fetal Programming
IUGR
Placenta
Preeclampsia
Journal
Clinical science (London, England : 1979)
ISSN: 1470-8736
Titre abrégé: Clin Sci (Lond)
Pays: England
ID NLM: 7905731
Informations de publication
Date de publication:
15 10 2021
15 10 2021
Historique:
received:
30
06
2021
revised:
08
09
2021
accepted:
29
09
2021
entrez:
13
10
2021
pubmed:
14
10
2021
medline:
15
12
2021
Statut:
ppublish
Résumé
Preeclampsia (PE), the leading cause of maternal and fetal morbidity and mortality, is associated with poor fetal growth, intrauterine growth restriction (IUGR) and low birth weight (LBW). Offspring of women who had PE are at increased risk for cardiovascular (CV) disease later in life. However, the exact etiology of PE is unknown. Moreover, there are no effective interventions to treat PE or alleviate IUGR and the developmental origins of chronic disease in the offspring. The placenta is critical to fetal growth and development. Epigenetic regulatory processes such as histone modifications, microRNAs and DNA methylation play an important role in placental development including contributions to the regulation of trophoblast invasion and remodeling of the spiral arteries. Epigenetic processes that lead to changes in placental gene expression in PE mediate downstream effects that contribute to the development of placenta dysfunction, a critical mediator in the onset of PE, impaired fetal growth and IUGR. Therefore, this review will focus on epigenetic processes that contribute to the pathogenesis of PE and IUGR. Understanding the epigenetic mechanisms that contribute to normal placental development and the initiating events in PE may lead to novel therapeutic targets in PE that improve fetal growth and mitigate increased CV risk in the offspring.
Identifiants
pubmed: 34643675
pii: 229932
doi: 10.1042/CS20190070
pmc: PMC8948502
mid: NIHMS1789397
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
2307-2327Subventions
Organisme : NIGMS NIH HHS
ID : P20 GM104357
Pays : United States
Organisme : NIGMS NIH HHS
ID : P20 GM121334
Pays : United States
Organisme : NHLBI NIH HHS
ID : R56 HL143459
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL143459
Pays : United States
Organisme : NHLBI NIH HHS
ID : P01 HL051971
Pays : United States
Organisme : NHLBI NIH HHS
ID : T32 HL105324
Pays : United States
Informations de copyright
© 2021 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.
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