Latest Articles

Publication Date
Chemokine CCL21 promotes the pathological progression of endometriosis by regulating inflammatory cytokine expression and activating the NF-κB signaling pathway.

Endometriosis, affecting approximately 10% of reproductive-aged women worldwide, is widely recognized as a chronic inflammatory disease. Inflammation-related genes (IRGs) play a crucial role in the occurrence and progression of various …

Published: June 29, 2026, midnight
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
Ovarian Endometriosis and Adenomyosis-Relevance, Pathophysiology of Ectopic Endometrium and Impact on Dysfunction of Eutopic Endometrium: A Narrative Review.

A trend toward comorbid conditions is seen in around 50% of gynecological patients, with a significant contribution made by endometriosis as a common and incurable gynecological condition. Over the last …

Published: June 13, 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
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
Targeting TLR4 Attenuates Endometriosis Progression by Suppressing NF-κB/NLRP3 Inflammasome Activation and Angiogenesis.

Endometriosis is a chronic inflammatory disorder affecting approximately 10% of reproductive-age women, yet non-hormonal therapeutic options remain limited. This study investigates the role of the TLR4/NF-κB/NLRP3 inflammasome axis in endometriosis …

Published: May 6, 2026, midnight
Integrative gene ontology-driven analysis of the eutopic endometrium reveals key dysregulated functionomes and pathways in endometriosis.

Endometriosis is a chronic estrogen-dependent inflammatory disorder associated with pelvic pain, infertility, and an increased risk of endometriosis-associated ovarian cancer. Despite extensive research, its molecular mechanisms remain incompletely understood. This …

Published: April 27, 2026, midnight
LRP1 as a potential diagnostic and immunomodulatory target in endometriosis: evidence from multi-omics and single-cell analyses.

Endometriosis (EMS) is a common gynecological disease that seriously affects women's health and quality of life. However, the detailed dynamic cellular and molecular mechanisms underlying EMS pathogenesis remain largely unknown. …

Published: April 15, 2026, midnight
Link copied to clipboard!
Subscribe to Our Newsletter

Stay updated with our latest articles!