ArticleFrontiers in immunology2026
PTN/IGF-2 signaling modulates endometrial decidualization and immune cell trafficking to facilitate pregnancy maintenance.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- PROK1 Expression Is Associated With Prognosis and May Influence Response to Antiandrogen Therapy in Prostate Cancer.Prostate cancer · 2026Article
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12 authors.
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Abstract
Background: Recurrent implantation failure (RIF) and recurrent pregnancy loss (RPL) are major causes of pathological early pregnancy, yet their mechanisms remain poorly understood. This study aimed to identify shared molecular mediators and their roles in endometrial dysfunction and immune regulation. Methods: Gene expression datasets for RIF and RPL were analyzed for differentially expressed genes (DEGs), functional enrichment, and protein-protein interaction (PPI) networks. Key regulators were identified using CytoHubba and Random Forest, and receiver operating characteristic (ROC) analysis evaluated their diagnostic performance. Endometrial stromal cells (ESCs) from RIF or RPL patients were used for Results: PPI network and machine learning analysis identified PTN as a central hub gene shared by RIF and RPL. ROC curves showed that PTN had the highest diagnostic value among all candidate genes. Immunofluorescence confirmed that PTN is mainly expressed in ESCs and downregulated in RIF and RPL patients. Discussion: The PTN/IGF-2 axis promotes ESC decidualization and a tolerogenic immune microenvironment, supporting endometrial receptivity. Dysregulation of this pathway may underlie pathological pregnancies (including RIF and RPL), highlighting PTN as a potential therapeutic target for early pregnancy loss.
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