ArticleJournal of assisted reproduction and genetics2025
Identification of shared pathogenetic mechanisms between endometriosis and RSA based on comprehensive bioinformatics analysis.
Article in Journal of assisted reproduction and genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- The diagnostic value and molecular mechanism of miR-199a-5p in recurrent spontaneous abortion.Journal of assisted reproduction and genetics · 2026Article
- Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeEndometriosis (EM) and recurrent spontaneous abortion (RSA) exhibit clinical associations, yet their shared molecular mechanisms remain unclear. This study aimed to identify shared molecular mechanisms and potential hub genes underlying EM and RSA.
methodsDifferentially expressed genes (DEGs) were identified from EM (GSE7305) and RSA (GSE165004) datasets. Functional enrichment and weighted gene co-expression network analysis (WGCNA) revealed shared pathways and key modules. Venny software was used to identify hub genes between DEGs and key module genes. The diagnostic value of FXYD1 was assessed via ROC analysis. Regulatory networks and immune cell infiltration were explored. Pan-cancer analysis was conducted to assess FXYD1's expression profile across tumor types. Single-cell RNA sequencing validated FXYD1 expression in EM tissues, maternal-fetal interface and RSA samples.
resultsDEGs in EM and RSA were enriched in pathways associated with abnormal proliferation, immune dysfunction, and developmental regulation. FXYD1 was identified as a shared hub gene, upregulated in both conditions, with potential diagnostic value. It was correlated with immune cell populations, particularly natural killer (NK) cells. Pan-cancer analysis revealed widespread FXYD1 downregulation across multiple cancer types. Single-cell RNA sequencing confirmed elevated FXYD1 expression in stromal and decidual cells of RSA tissues, implicating its role in impaired decidualization.
conclusionsFXYD1 emerges as a critical molecular link between EM and RSA, potentially contributing to decidualization dysfunction. Its dysregulation may underlie the shared pathophysiology of these conditions, offering new insights into their molecular mechanisms.
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