Placental exosomes in preeclampsia: unresolved questions in functional signaling and clinical translation

Preeclampsia is a hypertension condition unique to pregnancy that has a substantial global impact on maternal and fetal morbidity and mortality and is characterized by new-onset hypertension and proteinuria. The condition is caused by unusual placentation, leading to placental hypoxia and systemic endothelial dysfunction. Early prediction and effective targeted interventions are still limited. Exosomes and other extracellular vesicles are mediators of feto-maternal communication. These vesicles carry proteins, microRNAs, and other nucleic acids, detectable in maternal circulation. Total and placenta-derived exosomes are increased prior to the clinical onset of preeclampsia. Exosomal release caused by low oxygen levels leads to endothelial dysfunction and inflammatory signaling. Research focuses on exosome concentration instead of the functional impact of their molecular cargo. The specific effects of exosomes on maternal and fetal organ systems are not well understood. Future research should understand the systemic effects of exosomal communication and provide high-resolution analysis of its constituents. Applying research findings to clinical settings may allow earlier, non-invasive risk assessment and enhance outcomes in preeclampsia.