ArticleCellular & molecular biology letters2026
ENTPD3 as a novel regulator of endometrial receptivity: suppressing EMT via the ATP-P2Y2 axis in patients with recurrent implantation failure.
Article in Cellular & molecular biology letters, 2026. 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.
- Blastocyst-Derived Lactic Acid Regulates Uterine Epithelial Receptivity and Stromal Decidualization via the HIF1α-HO-1-Heme Metabolic Axis.Antioxidants (Basel, Switzerland) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
backgroundRecurrent implantation failure (RIF) remains a major challenge in assisted reproductive technology and is primarily attributed to impaired endometrial receptivity. Despite its clinical significance, the precise mechanisms underlying RIF remain inadequately understood.
methodsSingle-cell RNA sequencing (scRNA-seq) was performed on endometrial samples from patients with RIF and healthy controls during the secretory phase using the 10X Genomics Chromium platform. The expression and localization of ectonucleoside triphosphate diphosphohydrolase 3 (ENTPD3) in the window of implantation (WOI) in the endometrium were examined using real-time quantitative polymerase chain reaction (RT-qPCR), western blotting, and immunohistochemistry (IHC). A mouse model with ENTPD3 overexpression was utilized to assess embryo implantation in vivo, and an in vitro blastocyst adhesion assay was performed to evaluate endometrial receptivity. Additionally, Ishikawa cells were transduced with an ENTPD3 recombinant adenovirus to explore the underlying molecular mechanisms.
resultsENTPD3 expression was significantly upregulated in the endometria of patients with RIF during the WOI, and its apical surface localization in endometrial epithelial cells was confirmed by single-cell data and IHC. Functional studies demonstrated that ENTPD3 overexpression impaired endometrial receptivity by suppressing epithelial-mesenchymal transition (EMT). In vivo, ENTPD3 overexpression markedly reduced endometrial receptivity and inhibited embryo implantation in mice. Consistently, in vitro assays revealed that ENTPD3 overexpression diminished blastocyst adhesion to endometrial epithelial cells. Mechanistically, ENTPD3 hydrolyzes ATP, thereby suppressing EMT via the P2Y2 signaling pathway and ultimately disrupting endometrial receptivity.
conclusionsDysregulated ENTPD3 expression contributes to RIF pathogenesis by impairing endometrial receptivity through ATP hydrolysis-mediated suppression of EMT via P2Y2 signaling. These findings highlight ENTPD3 as a potential therapeutic target for improving implantation success in affected patients.
Indexed as
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.