title: Preeclampsia As Modulator of Offspring Health.
abstract: A balanced intrauterine homeostasis during pregnancy is crucial for optimal growth and development of the fetus. The intrauterine environment is extremely vulnerable to multisystem pregnancy disorders such as preeclampsia, which can be triggered by various pathophysiological factors, such as angiogenic imbalance, immune responses, and inflammation. The fetus adapts to these conditions by a mechanism known as developmental programming that can lead to increased risk of chronic noncommunicable diseases in later life. This is shown in a substantial number of epidemiological studies that associate preeclampsia with increased onset of cardiovascular and metabolic diseases in the later life of the offspring. Furthermore, animal models based predominantly on one of the pathophysiological mechanism of preeclampsia, for example, angiogenic imbalance, immune response, or inflammation, do address the susceptibility of the preeclamptic offspring to increased maternal blood pressure and disrupted metabolic homeostasis. Accordingly, we extensively reviewed the latest research on the role of preeclampsia on the offspring's metabolism and cardiovascular phenotype. We conclude that future research on the pathophysiological changes during preeclampsia and methods to intervene in the harsh intrauterine environment will be essential for effective therapies.
authors.affiliation: Department of Obstetrics and Gynecology, University of Groningen, University Medical Center Groningen, The Netherlands v.stojanovska@umcg.nl.
authors.forename: Violeta
authors.initials: V
authors.lastname: Stojanovska
authors.affiliation: Department of Obstetrics and Gynecology, University of Groningen, University Medical Center Groningen, The Netherlands.
authors.forename: Sicco A
authors.initials: SA
authors.lastname: Scherjon
authors.affiliation: Department of Obstetrics and Gynecology, University of Groningen, University Medical Center Groningen, The Netherlands.
authors.forename: Torsten
authors.initials: T
authors.lastname: Plösch
mesh_terms: D000818:Animals; D002648:Child; D005260:Female; D047109:Fetal Development; D006801:Humans; D011225:Pre-Eclampsia / Q000473:pathology*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects
keywords: early development; epigenetics; metabolism; preeclampsia