Latest Articles

Publication Date
Dysregulated Fas/Fas ligand expression in endometrial stromal cells and mononuclear cells in endometriosis.

Apoptosis plays a paramount role in endometriosis pathogenesis. This process may be disrupted in endometrial stromal cells (ESCs) of women with endometriosis, causing them to continue developing in ectopic locations. …

Published: June 22, 2026, midnight
Patient-derived eutopic and ectopic endometrial stromal cells: characterization and development of immortalized lines.

Ovarian endometriosis is an estrogen-dependent inflammatory disorder in which endometrial stromal cells are key cellular contributors to hormone-immune crosstalk and lesion persistence. Here, we isolated paired eutopic (NESC) and ectopic …

Published: June 19, 2026, midnight
TICAM1-Mediated TLR3/TLR4 Signaling Promotes Endometrial Stromal Cell Proliferation, Migration, and Invasion in Endometriosis via IRF3/IFN-β Axis.

Endometriosis (EMs) is an estrogen-dependent inflammatory disease characterized by the presence of endometrial-like tissue outside the uterine cavity, yet its precise pathogenesis remains incompletely elucidated. TICAM1, a key adaptor protein …

Published: June 4, 2026, midnight
RE-1 silencing transcription factor is reduced in endometriosis and uterine deletion in mice alters progesterone responsiveness.

Endometriosis is a steroid-dependent gynecologic disease characterized by progesterone (P4) resistance, subfertility/infertility, and pelvic pain; however, the molecular mechanisms underlying impaired P4 responsiveness in endometriosis tissue are not fully understood. …

Published: June 3, 2026, midnight
Endometriosis-Associated Infertility: A Review of Pathophysiological Mechanisms and Current Treatment Strategies.

Background: Endometriosis affects 10-15% of reproductive-aged women and is a leading cause of infertility through anatomical, inflammatory, and molecular mechanisms. Objective: This review synthesizes current evidence on the pathophysiology of …

Published: June 2, 2026, midnight
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
Single-cell profiling and machine learning identify cuproptosis-related fibroblast subpopulations and fibrogenesis modulator AEBP1 in endometriosis.

Endometriosis is characterized by progressive fibrosis and limited therapeutic options. Cuproptosis, a copper-dependent form of regulated cell death, has been implicated in multiple pathological conditions, but its relevance to fibroblast-mediated …

Published: May 18, 2026, midnight
Nuclear factor IX promotes endometriosis progression through transcriptional activation of tetraspanin-2.

Endometriosis is a benign yet aggressive disease characterized by enhanced proliferation and invasion of ectopic endometrial tissue. Identifying upstream regulators that co-regulate these processes will provide novel insights into endometriosis …

Published: May 16, 2026, midnight
Glycolytic reprogramming and MYH10 K1520 lactylation mediate eutopic endometrial collagen I deposition driven by PKM2-packaged ectopic endometrial extracellular vesicles.

Endometriosis (EMs) is characterized by ectopic lesions that disrupt endometrial decidualization, a process frequently accompanied by aberrant collagen deposition and closely linked to clinical infertility. Extracellular vesicles (EVs) are key …

Published: May 11, 2026, midnight
Altered miRNA cargo of endometrial extracellular vesicles in patients with endometriosis: potential implications for pregnancy outcomes.

Could the miRNA cargo of extracellular vesicles (EVs) secreted by eutopic endometrium from women with endometriosis be involved in the pregnancy complications related to endometriosis?

Published: May 7, 2026, midnight
Link copied to clipboard!
Subscribe to Our Newsletter

Stay updated with our latest articles!