ArticleTzu chi medical journal
Ovulatory follicular fluid promotes the clonogenicity and invasion of ectopic and eutopic endometrial cells.
Article in Tzu chi medical journal. 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.
- Phytochemicals Modulating Receptor Tyrosine Kinase Signaling Networks in Endometriosis.Pharmaceuticals (Basel, Switzerland) · 2026Review
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Authors and funding
9 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Objectives: Endometriosis is a chronic, estrogen-dependent disorder characterized by the ectopic growth of endometrial-like tissue. Despite its significant impact on fertility and quality of life, the pathogenesis of endometriosis remains poorly understood. This study investigates the potential role of ovulatory follicular fluid (FF) in driving disease progression. Based on the "double engines theory," which posits that retrograde menstruation provides the "seeds" for ectopic lesions while ovulation fuels their growth, we hypothesize that FF enhances endometrial cell proliferation, clonogenicity, migration, and invasion. Materials and Methods: Primary eutopic and ectopic endometrial cells were isolated from infertile women and treated with 10% diluted FF collected from Results: Morphological analysis revealed distinct adaptive changes, with ectopic cells predominantly adopting a more fibroblast-like phenotype. Ectopic cells exhibited higher clonogenicity (29.8-fold) capacities, lower proliferation (0.49-fold) and migration (0.11-fold) capacities, and similar invasion capabilities compared to eutopic cells. FF significantly enhanced proliferation (1.7-fold in eutopic and 1.3-fold in ectopic cells) and clonogenic capacity, with eutopic cells forming 31.3 times more colonies and ectopic cells showing a 1.3-fold increase. The clonogenic area expanded dramatically, increasing 261-fold in eutopic and 4.9-fold in ectopic cells. In addition, FF promoted migration (1.8-fold in eutopic and 2.9-fold in ectopic cells) and invasion (9.1-fold in eutopic and 4.8-fold in ectopic cells). These findings suggest that FF may play a pivotal role in the early establishment and progression of ectopic lesions. Conclusion: The results highlight the critical role of FF in enhancing endometrial cell survival, proliferation, and dissemination. This supports the "double engines theory" of endometriosis, emphasizing the significant contribution of ovulation to the pathogenesis of the disease.
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