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Placental Mitochondrial Function and Dysfunction in Preeclampsia

Authors :
Fahmida Jahan
Goutham Vasam
Alex E. Green
Shannon A. Bainbridge
Keir J. Menzies
Source :
International Journal of Molecular Sciences, Vol 24, Iss 4, p 4177 (2023)
Publication Year :
2023
Publisher :
MDPI AG, 2023.

Abstract

The placenta is a vital organ of pregnancy, regulating adaptation to pregnancy, gestational parent/fetal exchange, and ultimately, fetal development and growth. Not surprisingly, in cases of placental dysfunction—where aspects of placental development or function become compromised—adverse pregnancy outcomes can result. One common placenta-mediated disorder of pregnancy is preeclampsia (PE), a hypertensive disorder of pregnancy with a highly heterogeneous clinical presentation. The wide array of clinical characteristics observed in pregnant individuals and neonates of a PE pregnancy are likely the result of distinct forms of placental pathology underlying the PE diagnosis, explaining why no one common intervention has proven effective in the prevention or treatment of PE. The historical paradigm of placental pathology in PE highlights an important role for utero–placental malperfusion, placental hypoxia and oxidative stress, and a critical role for placental mitochondrial dysfunction in the pathogenesis and progression of the disease. In the current review, the evidence of placental mitochondrial dysfunction in the context of PE will be summarized, highlighting how altered mitochondrial function may be a common feature across distinct PE subtypes. Further, advances in this field of study and therapeutic targeting of mitochondria as a promising intervention for PE will be discussed.

Details

Language :
English
ISSN :
14220067 and 16616596
Volume :
24
Issue :
4
Database :
Directory of Open Access Journals
Journal :
International Journal of Molecular Sciences
Publication Type :
Academic Journal
Accession number :
edsdoj.0301b09e1a22458288b03474acfcd319
Document Type :
article
Full Text :
https://doi.org/10.3390/ijms24044177