ArticleReproductive sciences (Thousand Oaks, Calif.)2026
Novel Insights into the Pathogenic Role of CSF1R in Endometriosis.
Article in Reproductive sciences (Thousand Oaks, Calif.), 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
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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
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Who cites it
1 citing paper in PubMed.
- Bioinformatics and machine learning-driven discovery of candidate tissue diagnostic markers for endometriosis with experimental verification.Frontiers in endocrinology · 2026Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Endometriosis (EM) is a prevalent gynecological disorder linked to pelvic pain, menstrual disturbances, and infertility. Despite its clinical burden, the molecular mechanisms underlying EM remain elusive, necessitating the discovery of novel biomarkers and therapeutic targets. This study explored the role of colony-stimulating factor 1 receptor (CSF1R) in EM through an integrative approach combining bioinformatics and experimental validation. Differentially expressed genes (DEGs) were identified from the GSE11691 dataset using the limma package. Weighted Gene Co-expression Network Analysis (WGCNA) identified disease-associated gene modules. A Protein-Protein Interaction (PPI) network was constructed, and candidate genes were selected using Least Absolute Shrinkage and Selection Operator (LASSO) and Random Forest algorithms. Expression and function of CSF1R were validated in hEM15A cells via RT-qPCR, Western blotting, CCK-8, EdU, wound healing, and Transwell assays. WGCNA and PPI network analysis revealed a significant enrichment of genes within the PI3K/AKT/mTOR signaling pathway. Cross-validation using LASSO and Random Forest identified THBS2, CSF1R, IL-4R, and FLT1 as potential biomarkers. Among them, CSF1R was found to be significantly overexpressed in endometriotic stromal cells. Knockdown of CSF1R markedly suppressed cell proliferation, migration, and invasion, accompanied by decreased p-AKT expression. Rescue experiments using an AKT activator partially reversed these effects, supporting the functional role of CSF1R in modulating the AKT signaling pathway. CSF1R promotes the progression of endometriosis by modulating AKT signaling. It may serve as a valuable diagnostic biomarker and therapeutic target, providing new insights into endometriosis pathogenesis and treatment strategies.
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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 OpenQuestion graph.