A single-cell transcriptomics study of the fetal-maternal tissue interface in preeclampsia at different stages of gestation provides new information about the distinct maternal and fetal cell processes contributing to the serious pregnancy complication and points in the direction of potential therapeutic targets. By comparing fetal-maternal pairs with preeclampsia to healthy fetal-maternal pairs at similar stages of pregnancy, researchers at University College London found molecular signals of hypoxia, fibrosis, dysfunctional blood vessel formation and aberrant metabolism in placental cells from fetuses with severe preeclampsia. Transcriptomes of maternal tissues revealed molecular signatures of immune dysfunction in mitochondrial and interferon signaling, in tissues including the myometrium smooth muscle lining of the uterus and in the chorioamniotic membranes that surround a developing fetus. The researchers suggest these signals may contribute to systemic inflammation and impaired interactions with fetal cells. “This approach allowed us to detect novel signatures, such as mitochondrial signaling and interferon signaling in the placenta and other tissues of the fetal-maternal interface,” Sanchez-Corrales told BioWorld.