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O-GlcNAc modification regulates autophagy and apoptosis in endometriosis.

Endometriosis is a common, chronic gynecological disorder characterized by the presence of endometrial-like tissue outside the uterine cavity, frequently associated with significant morbidities such as pelvic pain and infertility. Elucidating …

Published: May 25, 2026, midnight
Molecular Characterization of Ovarian Endometriosis in Saudi Arabian Women: Insights into Inflammatory, Autophagic, and Epigenetic Dysregulation.

Ovarian endometriosis (OE) is a chronic, inflammatory gynecological disorder associated with sterility and an elevated risk of ovarian cancer. Despite its high prevalence, the complex molecular mechanisms governing OE pathogenesis …

Published: May 20, 2026, midnight
Hypoxia-mediated epigenetic silencing of YTHDF2 promotes endometriosis progression via the NFE2L1-NF-κB axis.

Endometriosis (EMs) is a chronic inflammatory disease characterized by ectopic growth of endometrial-like tissues. N6-methyladenosine (m6A) modification regulates diverse cellular processes, yet its role in EMs remains unclear. Here, we …

Published: May 19, 2026, midnight
Cancer-like Hallmarks of Endometriosis: The Role of Estrogen Signaling and Stem Cell Plasticity.

Endometriosis is a chronic estrogen-dependent inflammatory disease affecting approximately 10% of women of reproductive age and characterized by ectopic endometrial-like tissue growth. Although traditionally considered a benign gynecological condition, increasing …

Published: May 18, 2026, midnight
Advancing the frontiers of phytotherapy: a comprehensive review of botanical interventions targeting mitochondrial quality control to ameliorate endometriosis.

Endometriosis (EMs) is a gynecological disorder affecting women of reproductive age. It is characterized by the ectopic implantation and infiltration of endometrial-like tissue and is associated with significant effects on …

Published: April 29, 2026, midnight
Pelargonium graveolens Essential Oil Suppresses Proliferation and Migration and Modulates Mesenchymal-Associated Cellular Functions in Human Endometriotic Cells.

Endometriosis is characterized by enhanced cellular proliferation, migration, and resistance to apoptosis, contributing to lesion persistence and progression. Targeting cellular plasticity and mesenchymal-associated functions may therefore represent a promising therapeutic …

Published: April 15, 2026, midnight
In vitro exploration of the therapeutic potential of mesenchymal stem cell conditioned medium in endometriosis treatment by targeting apoptosis and cellular migration.

Endometriosis, a common gynecological disorder involving ectopic endometrial tissue, leads to infertility and chronic pain. Dysregulated apoptosis and abnormal cell migration are key pathological features. Given current treatment limitations, novel …

Published: April 15, 2026, midnight
CHCHD2: a bi-organellar fulcrum of mitochondrial homeostasis and reproductive pathology.

Mitochondrial dysfunction has been demonstrated with a role in pathologically driving various obstetric and gynecological (OB/GYN) diseases, but molecular mediators associating mitochondrial dysfunction with discrete pathologies have not been determined …

Published: April 13, 2026, midnight
Role of soluble EGFR, Fas, and Fas ligand in pelvic pain severity and their association with endometriosis in infertile woman: a case-control study.

Endometriosis, a chronic inflammatory condition linked to pelvic pain and infertility, is characterized by immune dysfunction involving dysregulated apoptosis and cell proliferation. This case-control study included 87 infertile women undergoing …

Published: April 8, 2026, midnight
Study on material basis and network mechanism of the Guizhi Fuling pills in the treatment of endometriosis and endometrial polyps.

To explore the material basis and network mechanism of the Guizhi Fuling pills in the treatment of endometriosis and endometrial polyps based on network pharmacology and machine learning. The effective …

Published: April 4, 2026, midnight
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