Angiogenic, Antiangiogenic Molecules, and Bioactive Lipids in Preeclampsia

Preeclampsia (PE) affects between 2% and 8% of pregnancies worldwide.¹ Risk factors for PE include obesity, prior hypertension, older age, and diabetes mellitus and is more likely to occur in first pregnancy and those who are carrying twins.^1,2 The underlying mechanism of PE is attributed to abnormal formation of placental blood vessels because of abnormal implantation and placentation. This leads to poor uterine and placental perfusion resulting in oxidative stress, hypoxic condition, and release of antiangiogenic factors such as soluble endoglin (sEng) and the soluble vascular endothelial growth receptor-1 (soluble Fms-like tyrosine kinase-1 [sFlt-1]), which induce endothelial dysfunction by inhibiting proangiogenic factors like placental growth factor (PIGF) and vascular endothelial growth factor (VEGF).^3–8 Despite its (PE) public health importance, no adequate preventive and management strategies are available except to terminate the pregnancy. Therefore, understanding the pathobiology of PE is important.

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