An international team of researchers has identified a molecular mechanism involved in ‘early preeclampsia’, a serious complication of pregnancy that can put the health of mother and baby at risk and, in the most severe cases, forces early delivery before the 34th week of gestation.
The work has been led by the Spanish Center for Molecular Biology Severo Ochoa -a joint center of the CSIC and the Autonomous University of Madrid- with the participation of researchers from the University of Melbourne and the Hospital Clínic-Hospital Sant Joan de Déu in Barcelona; the results have been published this Tuesday in the journal Cell Death and Disease.
Is it the cause of preeclampsia?
With our alarming maternal morbidity and mortality rates, and the statistic that 60% of #preeclampsia-related deaths are preventable, combating adverse outcomes starts with educating your patients and following best practices. https://t.co/DhFJJVNYFU pic.twitter.com/WVGeY7nOYYY
– Preeclampsia Foundation (@preeclampsia) April 8, 2026
The placenta is the organ that connects the mother with the fetus during pregnancy and allows the exchange of oxygen, nutrients and hormones necessary for the baby ‘s development and when its formation does not occur correctly, serious complications such as preeclampsia can occur, which puts maternal and fetal health at risk.
Its incidence, reported the CSIC in a press release, is estimated at between 5 and 10 percent of pregnancies, and despite the risk involved, the biological mechanisms that cause this pathology are not yet fully understood, and this is the context of the work led by researcher Vicente Pérez García, from the Center for Molecular Biology and the Príncipe Felipe Research Center in Valencia (east).
Using cellular and organoid models that simulate the early stages of placental development, researchers have discovered an abnormal increase in a protein (BAP1), essential in the early stage, which interferes with the normal formation of this maternal-fetal interface that is essential for proper embryonic development.
This alteration detected in vitro reproduces molecular characteristics observed in cases of ‘early preeclampsia’ and could help to better understand the mechanisms that trigger this disease.
The work has shown how the BAP1 gene, responsible for regulating the activity of other genes, plays a fundamental role in the maturation of the embryonic cells that will give rise to the placenta; its function is to facilitate the transition of these cells from an initial, still immature state to a specialized one capable of assuming the essential functions of the placenta.
The team used models based on human stem cells and three-dimensional organoids that recreate early stages of placental development, and the experiments showed that excessive levels of this protein prevent proper cell specialization and trigger changes associated with inflammation and immune response, characteristics that are also observed in ‘early preeclampsia’ placentas.
These changes are similar to those seen in women with early preeclampsia, such as reduced ability of the placenta to invade the uterus or problems in the layer responsible for maternal-fetal exchange, said Paula Doria-Borrell, a researcher at the Príncipe Felipe Research Center in Valencia and first author of the study.
The results reveal that precise control of this protein is essential for placental cells to specialize properly, since when this balance is lost, placental development is compromised.
Filed under: Cause of preeclampsia
With information from EFE
