Insight into the etiology of preeclampsia

Abstract

Ample amount of dietary aliments and inhaled oxygen transmission by the placenta and uterus blood stream is necessary by the mother and emerging fetus for their good health. Delicate equilibrium among the angiogenic growth activators and its receptors are responsible to reshape the spiral arteries, neoangiogenesis and the fetus development. Abnormal placentation in the beginning of pregnancy causes flawed reshaping the vessels of the uterus and releases numerous biological molecules in the maternal circulatory system, obstructing the balance among proangiogenic growth factors, such as, vascular endothelial growth factor (VEGF) or placental growth factor (PlGF) with antiangiogenic factors, like soluble form of fms-like tyrosine kinase-1 (sFlt-1) or endoglin (s-Eng). Inadequate placentation also secrete proinflammatory cytokines (such as TNF-a), oxygen deprived hypoxia-inducible factor (HIF), unstable reactive oxygen and nitrogen species (RONS), and autoantibodies against angiotensin type 1 receptors. There is also reduced generation of vasodilators, such as, nitric oxide (NO) and/ or prostacyclin. These alterations leading to inflammatory response, endothelial dysfunction and glomerular damage. Comorbidities present in mother, such as hypertension, diabetes mellitus, kidney ailments, antiphospholipid antibody syndrome, overweight, aging, or, a family history of pregnancy disorders are some of the notable risk factors. The vasculatures present in both placenta and maternal are important sources of RONS, a source of powerful pro-oxidants that can modify biomolecules and changes vascular activities in preeclampsia (PE). The sFlt-1/PlGF ratio is considered as an important risk identifier of PE development. Several therapeutics approaches are considered targeting angiogenic factors to treat preeclampsia; yet, placenta delivery is the ultimate definitive treatment.