Preeclampsia is a pregnancy-induced hypertensive disorder which affects about 5-7% of all pregnancies in the United States. Despite increased awareness of the disorder, it remains a leading cause of maternal and perinatal morbidity.
The underlying causes of the disorder are not clear, and there is currently no definitive treatment of the disease. The only definite intervention is delivery of the fetus and placenta. Treatment is largely confined to bed rest until the fetus has developed enough to allow for a safe delivery, though the health of the mother does not always permit this, making preeclampsia a leading cause of premature births. It is now recognized that the symptomatic phase of the disease is caused by the release of pathological factors from the placenta in response to hypoxia/ischemia. In the majority of preeclampsia cases, there is a failure of the vasculature to undergo remodeling which is necessary to ensure adequate delivery of blood to the placenta and maturing fetus. In response, the placenta becomes hypoxic, and this state causes the release of the above mentioned factors.
Our laboratory is interested in examining the link between placental ischemia and the production of these factors, such as the anti-angiogenic protein sFlt-1 and reactive oxygen. Further we are interested in the direct effect of these factors on the maternal endothelium. Currently, we are also examining the potential of the protein heme oxygenase-1 (HO-1) as a therapeutic in preeclampsia, through its documented ability to suppress sFlt-1 and reactive oxygen.
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Jackson, MS 39216
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