TY - JOUR
T1 - Syncytiotrophoblast stress in early onset preeclampsia
T2 - The issues perpetuating the syndrome
AU - Carrasco-Wong, Ivo
AU - Aguilera-Olguín, Macarena
AU - Escalona-Rivano, Rodrigo
AU - Chiarello, Delia I.
AU - Barragán-Zúñiga, L. Jazel
AU - Sosa-Macías, Martha
AU - Galaviz-Hernandez, Carlos
AU - San Martín, Sebastián
AU - Gutiérrez, Jaime
N1 - Publisher Copyright:
© 2021 Elsevier Ltd
PY - 2021/9/15
Y1 - 2021/9/15
N2 - Preeclampsia is a pregnancy-specific syndrome characterized by a sudden increase in blood pressure accompanied by proteinuria and/or maternal multi-system damage associated to poor fetal outcome. In early-onset preeclampsia, utero-placental perfusion is altered, causing constant and progressive damage to the syncytiotrophoblast, generating syncytiotrophoblast stress. The latter leads to the detachment and release of syncytiotrophoblast fragments, anti-angiogenic factors and pro-inflammatory molecules into maternal circulation, resulting in the emergence and persistence of the characteristic symptoms of this syndrome during pregnancy. Therefore, understanding the origin and consequences of syncytiotrophoblast stress in preeclampsia is vital to develop new therapeutic alternatives, focused on reducing the burden of this syndrome. In this review, we describe five central characteristics of syncytial stress that should be targeted or prevented in order to reduce preeclampsia symptoms: histological alterations, syncytiotrophoblast damage, antiangiogenic protein export, placental deportation, and altered syncytiotrophoblast turnover. Therapeutic management of these characteristics may improve maternal and fetal outcomes.
AB - Preeclampsia is a pregnancy-specific syndrome characterized by a sudden increase in blood pressure accompanied by proteinuria and/or maternal multi-system damage associated to poor fetal outcome. In early-onset preeclampsia, utero-placental perfusion is altered, causing constant and progressive damage to the syncytiotrophoblast, generating syncytiotrophoblast stress. The latter leads to the detachment and release of syncytiotrophoblast fragments, anti-angiogenic factors and pro-inflammatory molecules into maternal circulation, resulting in the emergence and persistence of the characteristic symptoms of this syndrome during pregnancy. Therefore, understanding the origin and consequences of syncytiotrophoblast stress in preeclampsia is vital to develop new therapeutic alternatives, focused on reducing the burden of this syndrome. In this review, we describe five central characteristics of syncytial stress that should be targeted or prevented in order to reduce preeclampsia symptoms: histological alterations, syncytiotrophoblast damage, antiangiogenic protein export, placental deportation, and altered syncytiotrophoblast turnover. Therapeutic management of these characteristics may improve maternal and fetal outcomes.
KW - Placenta
KW - Preeclampsia
KW - Stress
KW - Syncytiotrophoblast
UR - http://www.scopus.com/inward/record.url?scp=85106993646&partnerID=8YFLogxK
U2 - 10.1016/j.placenta.2021.05.002
DO - 10.1016/j.placenta.2021.05.002
M3 - Artículo
C2 - 34053733
AN - SCOPUS:85106993646
SN - 0143-4004
VL - 113
SP - 57
EP - 66
JO - Placenta
JF - Placenta
ER -