Abstract
Preeclampsia is a hypertensive disorder affecting 3–5% of all pregnancies. The only curative treatment is delivery of the placenta and the pathophysiology is poorly understood. Studies have demonstrated altered levels of antiangiogenic factors in patients with preeclampsia. One such factor is the antiangiogenic and antivasodilatatory peptide hormone vasoinhibin, which is higher in the circulation, urine, and amniotic fluid of women with preeclampsia. Normal pregnancy is characterized by elevated circulating prolactin and placental lactogen levels, both of which can serve as vasoinhibin precursors when they are enzymatically cleaved. A dysregulation of vasoinhibin generation during preeclampsia is indicated by higher vasoinhibin, prolactin, placental lactogen, and vasoinhibin-generating enzymes levels and activity. The present article integrates known vasoinhibin levels, effects, and signaling mechanisms to the clinical characteristics of preeclampsia to substantiate the notion that vasoinhibin dysregulation can be causally linked to the development of preeclampsia. If this view is demonstrated, assessment of vasoinhibin levels and regulation of its activity could help estimate the risk of preeclampsia and improve its treatment.
Highlights
Preeclampsia (PE) is a severe complication of pregnancy, defined by gestational hypertension and proteinuria after the 20th week of pregnancy [1]
vascular endothelial growth factor (VEGF) is a major promoter of angiogenesis and vasodilation in the placenta, and its actions are partially mediated by the production of endothelium-derived nitric oxide (NO)
Decreased levels of VEGF and NO occur in PE and inhibition of placental VEGF action and NO production causes reduced perfusion of the fetoplacental unit, hypertension, proteinuria, and fetal growth restriction, indicating that blockage of VEGF-induced NO production is causal in preeclampsia [42]
Summary
Preeclampsia (PE) is a severe complication of pregnancy, defined by gestational hypertension and proteinuria after the 20th week of pregnancy [1]. Vasoinhibin features a variety of endocrine, paracrine, and autocrine effects [25, 26] It is generated by matrix metalloproteinases (MMP), cathepsin-D, and bone morphogenic protein 1 (BMP-1) which cleave PRL in the region of the long loop connecting the third and fourth alpha helix [27,28,29]. In PE, the changes in circulating hormonal levels are altered compared to normal pregnancy, as are the level and activity of the cleaving enzymes determining the generation. The studies addressing vasoinhibin levels in PE, the changing values of their precursors, and the altered levels and activity of the cleaving enzymes have not been analyzed in conjunction with each other and with the altered physiology of the prolactin/vasoinhibin axis, the endocrine system that controls the generation and action of vasoinhibin [31].
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