Review: The potential role of placental extracellular vesicles in blood-brain barrier disruption and neuroinflammation in preeclampsia
- PMID: 40229181
- DOI: 10.1016/j.placenta.2025.04.001
Review: The potential role of placental extracellular vesicles in blood-brain barrier disruption and neuroinflammation in preeclampsia
Abstract
Preeclampsia is a complex pregnancy disorder characterized by hypertension and multisystem organ damage, notably affecting the liver, kidneys, and brain. Eclampsia, a severe form of preeclampsia, is marked by the sudden onset of generalized tonic-clonic seizures. Brain complications, including eclampsia, are responsible for 60-70 % of preeclampsia-related maternal deaths, particularly in low-income regions. Despite the significant impact of brain complications in preeclampsia, their underlying pathophysiology remains unclear. Evidence suggests that brain edema in preeclampsia and eclampsia results from disruption of the blood-brain barrier (BBB). Although direct analysis of the BBB is challenging, in vitro studies indicate that plasma from women with preeclampsia can compromise the BBB, with the specific circulating factors involved still unidentified. Among the potential culprits, recent findings highlight placental-derived small extracellular vesicles (PDsEVs) as key players in BBB disruption observed in preeclampsia. This review examines the role of PDsEVs in the pathophysiology of brain edema associated with preeclampsia, emphasizing areas for future research, including neuroinflammation and neuron dysfunction. Additionally, we discuss the protective role of magnesium sulfate in these processes.
Keywords: Blood-brain barrier; Extracellular vesicles; Preeclampsia (PE).
Copyright © 2025. Published by Elsevier Ltd.
Conflict of interest statement
Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:Carlos Escudero reports financial support and administrative support were provided by University of the Bio Bio. Carlos Escudero reports financial support was provided by National Agency for Research and Innovation (Chile). If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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