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Physiol Genomics. 2019 Mar 1;51(3):73-76. doi: 10.1152/physiolgenomics.00102.2018. Epub 2019 Feb 4.

Obesity "complements" preeclampsia.

Author information

1
Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University , Baton Rouge, Louisiana.
2
Reproductive Endocrinology & Women's Health Lab, Pennington Biomedical Research Center , Baton Rouge, Louisiana.

Abstract

Preeclampsia (PE) is a devastating adverse outcome of pregnancy. Characterized by maternal hypertension, PE, when left untreated, can result in death of both mother and baby. The cause of PE remains unknown, and there is no way to predict which women will develop PE during pregnancy. The only known treatment is delivery of both the fetus and placenta; therefore, an abnormal placenta is thought to play a causal role. Women with obesity before pregnancy have an increased chance of developing PE. Increased adiposity results in a heightened state of systemic inflammation that can influence placental development. Adipose tissue is a rich source of proinflammatory cytokines and complement proteins, which have been implicated in the pathogenesis of PE by promoting the expression of antiangiogenic factors in the mother. Because an aggravated inflammatory response, angiogenic imbalance, and abnormal placentation are observed in PE, we hypothesize that maternal obesity and complement proteins derived from adipose tissue play an important role in the development of PE.

KEYWORDS:

complement; immune; obesity; preeclampsia; pregnancy

PMID:
30716010
PMCID:
PMC6459374
[Available on 2020-03-01]
DOI:
10.1152/physiolgenomics.00102.2018

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