Aberrant maternal inflammation as a cause of pregnancy complications: A potential therapeutic target?

Abstract Pre-eclampsia (PE), fetal growth restriction (FGR), pre-term labour and fetal death are common complications of pregnancy often associated with abnormal maternal inflammation. Though the precise causes of these complications remain obscure, altered maternal blood flow to the placenta is an...

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Bibliographic Details
Published in:Placenta (Eastbourne) 2015-08, Vol.36 (8), p.960-966
Main Authors: Cotechini, T, Graham, C.H
Format: Article
Language:English
Subjects:
Animals
Female
Fetal death
Fetal growth restriction
Fetal Growth Retardation - pathology
Hemostasis
Humans
Inflammation
Inflammation - pathology
Internal Medicine
Nitric oxide
Nitroglycerin
Obstetrics and Gynecology
Oxidative stress
Placenta
Placenta - pathology
Pre-eclampsia
Pre-Eclampsia - pathology
Pre-term labour
Pregnancy
Pregnancy Complications - pathology
Spiral artery remodelling
Trophoblasts - pathology
Tumour necrosis factor
Utero-placental perfusion
Vasoconstriction
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Summary:Abstract Pre-eclampsia (PE), fetal growth restriction (FGR), pre-term labour and fetal death are common complications of pregnancy often associated with abnormal maternal inflammation. Though the precise causes of these complications remain obscure, altered maternal blood flow to the placenta is an underlying hallmark, especially with respect to the pathogenesis of PE, FGR and fetal demise. Furthermore, deficient trophoblast-mediated spiral artery remodelling is often cited as the primary cause of impaired utero-placental perfusion. Considerably less attention has been directed towards investigating other factors, including maternal vasoconstriction or hemostatic alterations, as contributors to poor utero-placental perfusion. This review provides a rationale for investigating the role of abnormal maternal inflammation in the pathophysiology of pregnancy complications including PE, FGR and fetal demise. In particular, the association between aberrant maternal inflammation and inadequate utero-placental perfusion is considered in the context of inflammation-associated alterations in maternal hemostasis and vasoconstriction. Finally, the role of aberrant maternal inflammation as a cause of local oxidative/nitrosative stress is examined and the possibility of targeting deficient nitric oxide signalling as a therapeutic intervention for the treatment of inflammation-associated pregnancy complications is discussed.
ISSN:0143-4004
1532-3102
DOI:10.1016/j.placenta.2015.05.016