Reference : Dysregulation of anti-angiogenic agents (sFlt-1, PLGF, and sEndoglin) in preeclampsia...
Scientific journals : Article
Human health sciences : Reproductive medicine (gynecology, andrology, obstetrics)
Dysregulation of anti-angiogenic agents (sFlt-1, PLGF, and sEndoglin) in preeclampsia--a step forward but not the definitive answer
Foidart, Jean-Michel mailto [Université de Liège - ULiège > Département des sciences cliniques > Gynécologie - Obstétrique - Labo de biologie des tumeurs et du développement >]
Schaaps, Jean-Pierre mailto [Université de Liège - ULiège > Département des sciences biomédicales et précliniques > Embryologie >]
Chantraine, Frédéric mailto [Université de Liège - ULiège > > Gynécologie-Obstétrique CHR >]
Munaut, Carine mailto [Université de Liège - ULiège > Département des sciences cliniques > Labo de biologie des tumeurs et du développement >]
Lorquet, Sophie mailto [Université de Liège - ULiège > > > Doct. sc. bioméd. & pharma. (Bologne) >]
Journal of Reproductive Immunology
Elsevier North Holland Biomedical Press
Yes (verified by ORBi)
[en] PE ; sFlt-1 ; sEndoglin ; Angiotensin 1 receptor auto-antibody ; Oxidative stress ; Inflammation
[en] Preeclampsia (PE) is a pregnancy-specific syndrome characterized by hypertension, proteinuria and edema, which resolves on placental delivery. It is thought to be the consequence of impaired placentation due to inadequate trophoblastic invasion of the maternal spiral arteries. In PE the maternal plasma concentration of free vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) is decreased whereas the concentration of soluble fms-like tyrosine kinase-1 (sFlt-1) and of soluble endoglin (sEng) is increased. These soluble receptors may bind VEGF, PLGF and TGFβ1 and TGFβ3 in the maternal circulation, causing endothelial dysfunction in many maternal tissues. Hence there is a view that the pathogenesis is more or less clarified. According to the vascular theory, poor placentation leads to poor uteroplacental perfusion and hypoxia, which stimulates sFlt-1 and sEng production causing the maternal syndrome. This assumption has been recently challenged. The role of hypoxia as the main stimulus for release of sFlt-1 has been questioned and the role of inflammatory mechanisms has been emphasized. According to this inflammatory theory, poor placentation may predispose more to placental oxidative stress than hypoxia and endothelial dysfunction may be part of a broader disorder of systemic inflammation. Finally, the recent demonstration of activating auto-antibodies to the angiotensin 1 receptor that experimentally play a major pathogenic role in PE further suggests a pleiotropism of aetiologies for this condition. The purpose of this review is to critically evaluate the recent hypotheses and their possible insights on early diagnosis, prevention and treatment.

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