ArticleJournal of clinical laboratory analysis2026
COL1A1
Article in Journal of clinical laboratory analysis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
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Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEndometritis is linked to adverse reproductive outcomes, but epithelial programs in disease initiation and persistence remain unclear. We aimed to systematically define inflammation-associated epithelial states and regulation in endometritis using single-cell analysis.
methodThe single-cell RNA sequencing (scRNA-seq) data from Gene Expression Omnibus (GEO) were processed using Seurat. After quality control, data were normalized with SCTransform and batch-corrected using the Harmony package. Cell types were annotated based on canonical markers. Differential expression analysis was performed to identify genes altered in endometritis. Epithelial cells were subsetted for reclustering and trajectory inference using Monocle2. Cell-cell communication was inferred with CellChat, and transcriptional regulon activity was assessed using SCENIC and AUCell methods.
resultsA total of 153,877 cells formed 14 clusters across seven lineages, with lower epithelial proportion in endometritis. Epithelial cells included four subpopulations (SPDEF
conclusionThis epithelial-centric single-cell atlas delineates disease-associated states, fate decisions, signaling axes, and regulatory programs in endometritis. The data support a model of epithelial fate remodeling coupled to angiogenic signaling and AP-1-driven transcription, nominating testable targets for mechanistic validation and potential translation.
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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 Socratic graph.