Our Group investigates the causes of preeclampsia through studying placentas and placental cells in the laboratory. We have been able to identify factors coming from the placenta that lead to damage in the mothers’ blood vessels and how this interaction can affect high cholesterol and other substances known to increase the risk of blood vessel and heart disease. We seek to develop new drug treatments for preeclampsia.
Our research goals are to better understand the causes of preeclampsia. By measuring the functions of the placenta and predicting preeclampsia, we seek to provide new, safe treatment which would allow the pregnancy to progress to full term, thus reducing the burden of premature delivery and also, long term, the risk to women’s heart health. Our work is directly translatable to women in pregnancy, resulting in an immediate impact through translational research efforts. Our Group has a strong international and national reputation for the quality and effect of our research plans. If preeclampsia could be prevented, then one of the strongest risk factors for women’s heart disease could also be prevented or reduced. This is an important long-term goal for women’s heart health.
Turanov AA, et al. RNAi modulation of placental sFLT1 for the treatment of preeclampsia. Nat Biotechnol. 2018.
Makris A, et al. Primate uteroplacental ischemia results in proteinuric hypertension and elevated placental and circulating sFLT-1. Circulation Research. 2006.
Makris A, et al. Placental growth factor reduces blood pressure in a uteroplacental ischemia model of preeclampsia in non-human primates. Hypertension. 2016.
Xu B, et al. Antihypertensive drugs methyldopa, labetalol, hydralazine, and clonidine improve trophoblast interaction with endothelial cellular networks in vitro. J Hypertens. 2014;32(5):1075-83; discussion 83.
Hennessy A, et al. A deficiency of placental IL-10 in preeclampsia. J Immunol. 1999;163(6):3491-5.