Abstract
Preeclampsia, a relatively common pregnancy disorder, is one of the major causes of maternal and fetal morbidity and mortality. Despite numerous research, the etiology of this syndrome remains not well understood as the pathogenesis of preeclampsia is complex, involving interaction between genetic, immunologic, and environmental factors. Preeclampsia, originating in placenta abnormalities, is induced by the circulating factors derived from the abnormal placenta. Recent work has identified various molecular mechanisms related to placenta development, including renin-angiotensin system, 1, 25-dihydroxyvitamin D, and lipoxin A4. Interestingly, advances suggest that vacuolar ATPase, a key molecule in placentation, is closely associated with them. Therefore, this intriguing molecule may represent an important link between various causes of preeclampsia. Here, we review that vacuolar ATPase works as a key link between multiple causes of preeclampsia and discuss the potential molecular mechanisms. The novel findings outlined in this review may provide promising explanations for the causation of preeclampsia and a rationale for future therapeutic interventions for this condition.
Highlights
Preeclampsia, a relatively common pregnancy disorder, is one of the major causes of maternal and fetal morbidity and mortality
SFlt1 can cause endothelial dysfunction in the maternal blood vessels by binding vascular endothelial growth factors and placental growth factor [4]; AT1-AA can react with the AT1 receptor in a stimulatory fashion similar to angiotensin II signalling, which could contribute to maternal hypertension [6]; MBG, involved in the pathogenesis of preeclampsia, has been demonstrated to cause hypertension, proteinuria, and intrauterine growth restriction in the rat model of preeclampsia [8]
What is the exact mechanism leading to deficient trophoblast invasion and further poor placenta? Immune responses and maternal endocrine system can be considered to be two main elements involved in the development of placenta
Summary
Preeclampsia, a pregnancy-complicated syndrome, is one of the leading causes of maternal and fetal morbidity and mortality [1]. SFlt can cause endothelial dysfunction in the maternal blood vessels by binding vascular endothelial growth factors and placental growth factor [4]; AT1-AA can react with the AT1 receptor in a stimulatory fashion similar to angiotensin II signalling, which could contribute to maternal hypertension [6]; MBG, involved in the pathogenesis of preeclampsia, has been demonstrated to cause hypertension, proteinuria, and intrauterine growth restriction in the rat model of preeclampsia [8] Augmented release of these factors secondary to the original poor placenta will eventually lead to damage of the endothelium, metabolism dysfunction, and inflammation as well as other typical symptoms. Progesterone plays a dominant role in maintaining uterine quiescence and modulating fetomaternal immune response locally, while estrogen appears to be a potent immunomodulator in pregnancy-associated immune function [10] Aberration in these hormones level may disrupt homoeostasis of placenta development, causing the onset of preeclampsia eventually. In the following the present review will focus on some new findings about interaction between V-ATPase and RAS, 1,25(OH)2D3 and lipoxin A4 in pregnancy, which will provide new insights into the molecular mechanisms underlying preeclampsia
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