Latest Articles

Publication Date
SEMA3C Promotes the Progression of Endometriosis by Inducing Ferroptosis and Enhancing the Viability and Migration of Endometrial Stromal Cells.

Endometriosis (EMs) is a chronic inflammatory disorder involving ectopic endometrial-like tissue. Semaphorin 3C (SEMA3C), a secreted guidance protein regulating cell survival, migration, and tissue remodeling, may contribute to EMs. This …

Published: Sept. 1, 2026, midnight
Study on the role of miR-433-3p in the occurrence and development of endometriosis.

This study aims to characterize the expression pattern and biological functions of miR-433-3p in endometriosis. Eutopic and ectopic endometrial tissues were collected from endometriosis patients, and the expression level of …

Published: Aug. 21, 2026, midnight
Single-Cell RNA Sequencing Shows Markedly Elevated Immune Cell Proportions in the Endometrium of Women with Endometriosis-A Narrative Review.

Single-cell RNA sequencing is a state-of-the-art approach to decipher the heterogeneity of RNA transcripts in individual cells and identify different cell types in tissues and organs. Its aim is to …

Published: Aug. 20, 2026, midnight
Exosomal miR-21-5p from ectopic endometrial stromal cells drives fibrosis progression in endometriosis through direct VHL targeting.

Ovarian endometriosis is a chronic inflammatory disease characterized by extensive tissue remodeling and fibrosis, which significantly impacts female reproductive health. This study demonstrates that ectopic endometrium (Ect) in patients with …

Published: Aug. 12, 2026, midnight
FOSL2-driven SASP in endometrial stroma promotes the inflammation of endometriosis.

Endometriosis (EMs) is characterized by chronic pelvic inflammation, but the etiology of this inflammation remains poorly understood. The senescence-associated secretory phenotype (SASP), whereby senescent cells secrete pro-inflammatory cytokines, is a …

Published: July 24, 2026, midnight
Yiqi Huoxue Formula ameliorates endometriosis by suppressing NF-κB p65/NLRP3 inflammasome-associated pyroptotic signaling.

Yiqi Huoxue Formula (YQHXF) is an 11-herb hospital-based traditional Chinese medicinal formula developed according to the therapeutic principle of tonifying qi and activating blood circulation. Previous clinical application has suggested …

Published: July 14, 2026, midnight
Metabolic remodeling of endometriosis microenvironment: Energy stress and immune evasion.

Endometriosis (EMs) is an estrogen-dependent chronic inflammatory gynecological disease characterized by ectopic growth of endometrial tissues, leading to dysmenorrhea, pelvic pain, and infertility. Although the retrograde menstruation theory clarifies the …

Published: July 9, 2026, midnight
FIN56-induced ferroptosis suppresses the development of endometriosis by augmenting mitochondrial ROS and lipid peroxidation via the ACACA/ARID5A/NOX4 axis.

Endometriosis (EMs) is one of the most common gynecologic diseases, and the roles of ferroptosis in EMs have not been fully clarified. The induction of ferroptosis has been demonstrated to …

Published: June 29, 2026, midnight
Macrophage-derived exosomes promote proliferation, migration, and invasion of endometrial stromal cells in endometriosis and are associated with exosomal lncRNA ZFAS1: A pilot translational study.

Endometriosis (EMs) is a prevalent gynecological disorder affecting reproductive-age women. Exosomes secreted by peripheral blood macrophages may participate in EMs progression. In this pilot translational study, exosomes from peripheral blood …

Published: June 24, 2026, midnight
Three-Dimensional Organoid-like Co-Culture of Human Endometrial Endothelial and Stromal Cells to Study Endometriosis-Associated Responses.

Three-dimensional (3D) endothelium-stromal co-cultures were established using human endometrial cells from biopsy of healthy women (n = 13) and serum samples from both healthy and endometriotic women (n = 5). …

Published: June 23, 2026, midnight
Link copied to clipboard!
Subscribe to Our Newsletter

Stay updated with our latest articles!