From inhibition of trophoblast cell invasion to proapoptosis: what are the potential roles of kisspeptins in preeclampsia?

Preeclampsia (PE) is a life-threatening human gestational syndrome with incompletely understood etiopathogenesis. The disorder has a spectrum of clinical features, likely due to a complex interaction between maternal predisposing factors and abnormalities at the maternal-fetal interface. Poor trophoblast cell invasion, inadequate uterine vascular remodeling, and placental hypoperfusion are considered as key placental events leading to PE. Kisspeptins, a family of small peptides derived from the KISS1 gene, have been implicated in the development of this syndrome. Most studies of kisspeptin expression in PE have reported an upregulation of kisspeptins and/or their cognate receptor in preeclamptic placentas. Conversely, maternal peripheral blood concentration of kisspeptins is reportedly lower in PE than in uncomplicated pregnancies. This apparent paradox remains to be further elucidated. Although kisspeptins were initially known for inhibiting cellular migration and invasion, other biological activities attributed to these peptides include neuroendocrine regulation of reproduction, metabolism regulation, inhibition of angiogenesis, and induction of apoptosis. This review summarizes the current knowledge on expression and biological activity of kisspeptins at the maternal-fetal interface in the context of PE.

Automated summary

Preeclampsia is a life-threatening pregnancy complication with incompletely understood causes, possibly due to a complex interaction at the maternal-fetal interface. Inadequate trophoblast invasion, insufficient uterine vascular remodeling, and poor placental perfusion are key events leading to this syndrome.