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Repurposing ramipril to mitigate EMT-like transition in endometriosis by PI3K/AKT/S6K1 signalling pathway: a study in endometriosis induced rats.

Endometriosis, an atypical benign disorder, may disrupt epithelial-mesenchymal transition (EMT) due to a dysregulated balance between matrix metalloproteinases (MMPs) and their inhibitors. Ramipril, an angiotensin converting enzyme (ACE) inhibitor, is …

Published: Jan. 28, 2026, midnight
CXCL12 promotes EMT-mediated malignant transformation of endometriosis-associated ovarian cancer via PI3K/Akt signaling: An integrated transcriptomic and clinical study.

Endometriosis-associated ovarian cancer (EAOC) is a distinct form of epithelial ovarian cancer that arises from the malignant transformation of benign endometriotic lesions. While epithelial-mesenchymal transition (EMT) is acknowledged as a …

Published: Jan. 16, 2026, midnight
Correlation between Polycomb repressive complex proteins and epithelial-mesenchymal transition-associated genes in endometriotic tissues.

Endometriosis is a condition in which functional endometrial glands and stroma are found to grow outside the uterine cavity that can lead to symptoms like dysmenorrhea, dyspareunia, adhesions, and infertility. …

Published: Dec. 19, 2025, midnight
Di-(2-ethylhexyl) phthalate induces endometriosis by modulating IGF-1 m6A methylation via the intestinal Odoribacter-butyric acid axis in female rats.

Endometriosis, a complex gynecological disorder characterized by aberrant growth of endometrial tissue outside the uterine cavity, poses a significant challenge to women's health. Emerging evidence implicates environmental pollutants, particularly di-(2-ethylhexyl) …

Published: Sept. 23, 2025, midnight
C57BL/6J mice best recapitulate fibrosis and inflammatory pathophysiology in syngeneic mouse model of endometriosis.

Endometriosis (ENDO), a chronic inflammatory disease affecting approximately 190 million women globally, is characterized by fibrosis, a feature often challenging to replicate in murine models. To identify an optimal syngeneic …

Published: Aug. 8, 2025, midnight
Corrigendum to "The role of miR-34c-5p/Notch in epithelial-mesenchymal transition (EMT) in endometriosis" [Cellular Signalling, August 2020, Volume 72, 109666].

Published: April 8, 2025, midnight
A new perspective on endometriosis: Integrating eQTL mendelian randomization with transcriptomics and single-cell data analyses.

Endometriosis is caused by the migration of endometrial cells to locations outside the uterine lining. Despite the increasing prevalence of endometriosis, there has been limited research on genetic effects, and …

Published: March 26, 2025, midnight
Expression of E-CADHERIN and miR-200b in Different Forms of Endometriosis.

Background/Objectives: Epithelial-Mesenchymal Transition (EMT) is the process by which epithelial cells acquire mesenchymal properties, which helps endometriotic cells migrate and invade. This study looks at the expression of E-CADHERIN, a …

Published: Feb. 19, 2025, midnight
Potential Modulatory Role of Phoenixin-14 in Epithelial-Mesenchymal Transition of Endometriotic 12Z Cells.

Background/Objectives: Endometriosis is a painful chronic condition in which the endometrium grows outside the uterus. The epithelial-mesenchymal transition (EMT) is critical to endometriosis progression, where cells lose epithelial traits and …

Published: Jan. 10, 2025, midnight
[Fibrosis signaling in endometrial cells and endometriosis development].

In endometriosis, the tissues similar to the endometrial tissue attaches outside the uterine cavity, causing inflammation and fibrosis. The retrograde menstruation theory is the most plausible mechanism, though the detailed …

Published: Nov. 6, 2024, midnight
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