Pregnancy Hypertension: An International Journal of Women's Cardiovascular Health
ReviewTrophoblast differentiation, fetal growth restriction and preeclampsia
Section snippets
Trials to define preeclampsia
The exact etiology of the pathogenesis of preeclampsia is still unclear and remains a subject of extensive research even today. Although a multifactorial background is anticipated, it has become clear that the placenta rather than the fetus is a prerequisite for the development of the syndrome. Beside the crucial role of the placenta in the etiology of preeclampsia, the maternal response and susceptibility to placentally derived factors and proteins further modifies onset, severity and
Trophoblast differentiation
At about six days post conception (pc) when the morula develops into the blastocyst, trophoblast is the first cell lineage to differentiate during human embryonic development. During the next two weeks subsequent differentiation steps culminate in the formation of the two different populations of trophoblast, villous and the extravillous trophoblast [7].
Villous trophoblast with its two layers, villous cytotrophoblast and syncytiotrophoblast, already develops as soon as the first villi grow from
Serum markers to predict preeclampsia and FGR
As in other clinical sciences there is a general trend in obstetrics and perinatal medicine to focus on early predictive markers. Early prediction allows for setting up and planning appropriate management of pregnant women at high risk, even opening up the avenue for testing putative preventative measures to improve overall outcome. So far, putative therapies can only be started at the time of detection of clinical symptoms of preeclampsia and/or FGR [1], [2], [14], [15]. However, early
Placental origins of preeclampsia and FGR
The last decades have seen a variety of hypotheses that have been generated aiming to explain the placental origins of preeclampsia [34], [35], [36], [37] with most of them disappearing soon while a few are still discussed and are updated continuously [38]. Today it has become clear that preeclampsia does not originate in midgestation but rather the etiology needs to be located during very early stages of pregnancy [39]. The change in view also challenged one of the hypotheses that is still
Conclusions
The adaptations and updates of hypotheses to explain the etiology of FGR and preeclampsia continue. However, even after the update this hypothesis still clearly separates the origins of FGR and preeclampsia. It becomes obvious that the two syndromes are indeed different entities. Studies where preeclampsia cases with and without FGR are mixed will not help in elucidating the origins of both syndromes. Only a thorough analysis and comparison of both syndromes can decipher their similar but
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