Epigenetic processes during preeclampsia and effects on fetal development and chronic health

Usman M Ashraf, Dalton L Hall, Adam Z Rawls, Barbara T Alexander, Usman M Ashraf, Dalton L Hall, Adam Z Rawls, Barbara T Alexander

Abstract

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.

Keywords: Epigentics; Fetal Programming; IUGR; Placenta; Preeclampsia.

Conflict of interest statement

Competing Interests

The authors declare that there are no competing interests associated with the manuscript.

© 2021 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.

Figures

Figure 1.. The pathogenies of IUGR
Figure 1.. The pathogenies of IUGR
Summary of the effects of placental ischemia on fetal growth and how adaptive changes in epigenetic regulations such as DNA methylation, miRNAs and histone modifications as the result of placenta ischemia result in IUGR in offspring.

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