ArticleCell reports. Medicine2025
Type I interferon exposure of an implantation-on-a-chip device alters invasive extravillous trophoblast function.
Article in Cell reports. Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Spatially resolved fetal and maternal cell contributions to severe preeclampsia across gestation.Science advances · 2026Article
- The pro-inflammatory cytokines IFN-α and TNF-α inhibit organoid-derived extravillous trophoblast invasion.iScience · 2026Article
- Recent advances in sex-specific reproductive microphysiological systems for the systematic evaluation of assisted reproductive technology.Materials today. Bio · 2026Review
- Single-cell transcriptomic landscape of the mid-secretory eutopic endometrium reveals receptivity defects in adenomyosis.Journal of translational medicine · 2026Article
- Targeting pathogenic interferon-stimulated gene RSAD2 improves pregnancy outcomes in systemic lupus erythematosus models.Cell reports. Medicine · 2025Article
- Congenital Zika virus infection in laboratory animals: a comparative review highlights translational studies on the maternal-foetal interface.Memorias do Instituto Oswaldo Cruz · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Inappropriate type I interferon (IFN) signaling during embryo implantation and placentation is linked to poor pregnancy outcomes. Here, we evaluate the consequence of elevated type I IFN exposure on implantation using a human implantation in an organ-on-a-chip device. We reveal that type I IFN reduces extravillous trophoblast (EVT) invasion capacity. Analyzing single-cell transcriptomes, we uncover that IFN truncates invasive EVT emergence in the implantation-on-a-chip device by stunting EVT epithelial-to-mesenchymal transition. Disruptions to the epithelial-to-mesenchymal transition are associated with the pathogenesis of preeclampsia, a life-threatening disorder of pregnancy. Strikingly, IFN stimulation induces genes associated with increased preeclampsia risk in EVTs. These dysregulated EVT phenotypes ultimately reduce EVT-mediated endothelial cell vascular remodeling in the implantation-on-a-chip device. Overall, our work implicates unwarranted type I IFN as a maternal disturbance that can result in abnormal EVT function that could trigger preeclampsia.
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Registered trials
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