ArticleScientific reports2025
Multi-omics analysis reveals shared diagnostic and therapeutic targets in endometriosis and recurrent implantation failure.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Embryonic Mediators of Embryo-Uterus Communication, Implantation and Pregnancy.Molecular reproduction and development · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
Endometrial receptivity is essential for successful pregnancy, and endometriosis is widely recognized as a disruptor of this process. Poor endometrial receptivity is also a key factor contributing to recurrent implantation failure. Although some molecular mechanisms related to endometrial receptivity have been identified, their specific roles in endometriosis and recurrent implantation failure remain unclear. This study aimed to elucidate the shared molecular mechanisms affecting endometrial receptivity in endometriosis and recurrent implantation failure using multi-omics data analysis. We sourced datasets from the NCBI GEO database and employed weighted gene co-expression network analysis to identify gene modules associated with these conditions, followed by gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. Single-cell sequencing analysis and immunofluorescence were used for expression analysis. We identified 3690 and 4892 upregulated genes and 2675 and 5065 downregulated genes in endometriosis and recurrent implantation failure, respectively. Functional enrichment analysis and validation identified 15 hub genes including SRPRB, SLC35B1, and SLC25A6. Receiver operating characteristic curve analysis demonstrated that these genes are associated with high diagnostic accuracy. Single-cell sequencing analysis indicated that these genes are predominantly expressed in basal epithelial cells, with RBM3 being particularly prominent. This study provides new insights into the molecular mechanisms underlying endometrial receptivity and identifies potential targets for the diagnosis and treatment of endometriosis and recurrent implantation failure.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.