ArticleCell death discovery2025
GM-CSF improves the receptivity of thin endometrium by promoting glandular and stromal cell proliferation in mice and humans.
Article in Cell death discovery, 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.
- Molecular pathways and immune microenvironment regulation in stem cell therapy for thin endometrium: a comprehensive narrative review.Frontiers in immunology · 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
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thin endometrium (TE, ≤7 mm) is widely recognized as a critical cause of infertility, recurrent pregnancy losses, and placental abnormalities. Granulocyte-macrophage colony-stimulating factor (GM-CSF) plays a crucial role in tissue repair, but its effect on endometrial regeneration has been less investigated. We employed a thin endometrium mouse model established through unilateral 95% ethanol injury in an animal study and thin endometrium patients in a parallel clinical study. Both mice and patients were randomly apportioned into two groups: the Saline group and the GM-CSF group. We demonstrate that GM-CSF significantly increases endometrium thickness and gland number, promotes the proliferation of stromal cells, and improves the number of embryo implantation sites in the mouse model (P < 0.05). GM-CSF significantly (P < 0.05) promotes the proliferation of glandular cells, but not stromal cells in humans due to species-specific differential effects. GM-CSF treatment in humans induces upregulation of tissue repair/regeneration genes and enrichment of angiogenesis, cell adhesion, and epithelial proliferation pathways at the transcriptional level. The pregnancy outcomes, implantation rate (24.10% vs. 17.39%), and clinical pregnancy rate (34.78% vs. 26.32%), were both enhanced by GM-CSF compared to the Saline group. The delivery rate shows no statistically significant discrepancy between the two groups. GM-CSF has a positive role in endometrial regeneration and pregnancy outcomes in a thin endometrium. In conclusion, our study provides a novel therapeutic approach for thin endometrium and related infertility.
Identifiers
What OpenQuestion 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 OpenQuestion graph.