ArticleBiology2025
Immune Dysregulation and Trophoblastic Dysfunction as a Potential Cause of Idiopathic Recurrent Pregnancy Loss.
Article in Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
The trial behind it
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.
- Review
- Arginine methyltransferase PRMT1 equipoises trophoblast development to prevent early pregnancy loss.Nature communications · 2026Article
- Gestational Dynamics of Hofbauer Cells in the Human Placenta: Distribution, Morphology, and Immunophenotype.Journal of developmental biology · 2026Article
- Artificial Intelligence in Recurrent Pregnancy Loss: Current Evidence, Limitations, and Future Directions.Journal of clinical medicine · 2026Review
- Maternal-fetal interface abnormalities in unexplained recurrent pregnancy loss: mechanisms, models, and a framework for subtype identification.Frontiers in endocrinology · 2026Review
- Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Recurrent pregnancy loss (RPL) is a multifactorial condition affecting 1-5% of couples, often with unclear etiology. Idiopathic pregnancy losses (iPLs) are particularly challenging due to unknown molecular mechanisms. This study investigates the transcriptomic profiles of first-trimester products of conception (POC) from iPLs to uncover underlying molecular pathways. We performed RNA-sequencing on nine POC samples, identifying two distinct clusters enriched in trophoblast and decidual cells. Deconvolution analysis revealed reduced syncytiotrophoblast (STB) cells, with increased cytotrophoblast (CTB) and extravillous trophoblast (EVT) cells in iPLs. Gene Set Enrichment Analysis highlighted immune pathways enrichment in both villous trophoblasts and decidua. Gene ontology (GO) analysis of downregulated genes implicated hormonal and endocrine processes, consistent with STB reduction, while upregulated genes were associated with MHC protein complex and immune system processes, aligning with EVT increases. Histological analysis showed chronic histiocytic intervillositis (CHI) in iPL samples, supporting maternal immune dysregulation in unexplained RPL. Together, transcriptomic and histological analyses indicate that immune signaling dysregulation and impaired trophoblast differentiation may underlie unexplained iPLs. These findings bridge molecular and histopathological evidence, underscoring the interplay between trophoblast dysfunction and immune imbalance. Our results provide insights into iPL pathogenesis, highlighting potential biomarkers that may contribute to improved diagnosis and future research.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.