Preeclampsia: multiple approaches for a multifactorial disease

Kathleen A Pennington,Daniel L Jackson,Laura C Schulz,Jessica M Schlitt,Danny J Schust

doi:10.1242/dmm.008516

Kathleen A Pennington, Daniel L Jackson + Show 3 more

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https://doi.org/10.1242/dmm.008516

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Journal: Disease Models & Mechanisms	Publication Date: Dec 28, 2011
Citations: 249	License type: cc-by

Affiliation: University of Missouri

Abstract

Preeclampsia is a pregnancy-specific disorder characterized by hypertension and excess protein excretion in the urine. It is an important cause of maternal and fetal morbidity and mortality worldwide. The disease is almost exclusive to humans and delivery of the pregnancy continues to be the only effective treatment. The disorder is probably multifactorial, although most cases of preeclampsia are characterized by abnormal maternal uterine vascular remodeling by fetally derived placental trophoblast cells. Numerous in vitro and animal models have been used to study aspects of preeclampsia, the most common being models of placental oxygen dysregulation, abnormal trophoblast invasion, inappropriate maternal vascular damage and anomalous maternal-fetal immune interactions. Investigations into the pathophysiology and treatment of preeclampsia continue to move the field forward, albeit at a frustratingly slow pace. There remains a pressing need for novel approaches, new disease models and innovative investigators to effectively tackle this complex and devastating disorder.

Highlights

Preeclampsia is the most common hypertensive disease of pregnancy, affecting 5-8% of pregnancies (Saftlas et al, 1990) and accounting for nearly 18% of maternal deaths (ACOG, 2002) in the United States
Preeclampsia is associated with adverse fetal outcomes, including intrauterine growth retardation (IUGR), placental abruption, oligohydramnios and non-reassuring fetal surveillance
HELLP syndrome is a specific variant of severe preeclampsia

Summary

Introduction

Preeclampsia is the most common hypertensive disease of pregnancy, affecting 5-8% of pregnancies (Saftlas et al, 1990) and accounting for nearly 18% of maternal deaths (ACOG, 2002) in the United States. An ideal animal model of this disease would exhibit all the symptoms seen in women with preeclampsia, including hypertension, proteinuria, endothelial dysfunction and an imbalance of angiogenic factors, all of which arise secondary to poor trophoblast invasion and resolve following delivery of the placenta (McCarthy et al, 2011a).

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Conclusion