Abstract
Preeclampsia is the major cause of both maternal and neonatal morbidity and mortality. Its insidence remains high and the management has not been established yet because its etiology and pathophysiological are still poorly understood. Theories regarding etiopathogenesis and management of preeclampsia have been postulated yet it remains controversial. Placental ischemic and angiogenic imbalance are suggested to be predisposing factors of preeclampsia. It is thereby targeted in prevention of preeclampsia. Unfortunately, both primary and secondary prevention using various supplements and drugs fails to exhibit good outcome. Overall, these efforts are considered useless. In recent years, researchers have been using statin derivative in management of preclampsia. It has been reported that statin provides protective effect in endothelial cells by inducing expression of Hmox-1 and inihibiting release of sFlt-1 as well as potent antioxidant properties. Thus, statin has been proposed as promising agent to significantly reduce anti-angiogenic in preeclamptic patients which is overviewed in this review based on recent studies.
Highlights
Preeclampsia is known to contribute to 5% pregnancy and major cause in maternal mortality (24%) after hemorrhage (28%)
It has been reported that statin provides protective effect in endothelial cells by inducing expression of Heme oxygenase (Hmox)-1 and inihibiting release of sFlt-1 as well as potent antioxidant properties
Angiogenic imbalance in preeclampsia caused by elevated sFlt-1 and sEng that results in decreased PlGF and VEGF, affects Hmox-1 level in regulating biological process in human
Summary
Preeclampsia is known to contribute to 5% pregnancy and major cause in maternal mortality (24%) after hemorrhage (28%). Elevated sFlt-1 generates endothelial damage and inhibits angiogenesis by binding of has a antagonist role toward VEGF and P1GF, increase oxidatove stress and inflammation, whilst elevated sEng (soluble Endoglin) in preeclampsia limits signal transduction of TGFβ1. Carbon monoxide is a strong vasolidator that maintains angiogenic balance by inhibiting sFlt and sEng, as well as increasing P1GF and VEGF. Angiogenic imbalance in preeclampsia caused by elevated sFlt-1 and sEng that results in decreased PlGF and VEGF, affects Hmox-1 level in regulating biological process in human. This event indicates down regulation of antioxidant Hmox-1 which is correlated to pathogenesis of preeclampsia in placenta [11,12,13,14]. Prevention of preeclampsia has not provided good result [15,16]
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