Latest Articles

Publication Date
ZNF143 Promotes Endometriotic Lesion Growth and Fibrosis through the Plasminogen Activator Inhibitor-1 Pathway.

Endometriosis (EMs) is a chronic, estrogen-dependent gynecological disorder characterized by the ectopic growth of endometrial tissue outside the uterus. Zinc Finger Protein 143 (ZNF143) is a DNA-binding transcription factor, yet …

Published: June 18, 2026, midnight
RNF34 restrains endometriosis through SREBP1-dependent metabolic-immune crosstalk.

Endometriosis is a chronic inflammatory disease with cancer-like features, yet the mechanisms linking metabolic dysregulation to immune remodeling during lesion progression remain poorly understood. Here, we identify the ubiquitin E3 …

Published: June 13, 2026, midnight
Breaking the endometriosis-stroke axis: lesion-focused hydrogel reprogramming of thromboinflammatory networks.

Endometriosis is a chronic, systemic inflammatory disorder characterized by the ectopic implantation of endometrial-like tissue and accompanied by persistent pain and infertility. Beyond the pelvis, accumulating epidemiological evidence indicates that …

Published: June 8, 2026, midnight
Anti-NRP1 peptide-engineered ROS/pH dual-responsive nanoparticles for Alpelisib delivery regulate Sema3A-NRP1/PI3K-AKT signaling to balance oxidative stress and inhibit angiogenesis in endometriosis.

Endometriosis progression is driven by oxidative stress and excessive angiogenesis within an inflammatory microenvironment. To overcome these challenges, we designed ROS/pH dual-responsive Alpelisib-loaded nanoparticles (Alp@TAT-AT7-NPs) functionalized with an anti-NRP1 peptide …

Published: June 6, 2026, midnight
Gut microbiota dysbiosis in endometriosis: mechanistic insights and gut microbiota-targeted therapeutic strategies.

Endometriosis (EMs) is a prevalent, estrogen-dependent gynecological disorder characterized by the ectopic implantation and proliferation of endometrial-like tissue outside the uterine cavity, affecting approximately 10% of reproductive-aged women globally. Despite …

Published: June 5, 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
PBMC-derived FGF, PDGF, VEGF and GM-CSF secretion in endometriosis: a case-control in vitro study.

Endometriosis is a chronic inflammatory disease with immune dysregulation in which angiogenic, and hematopoietic mediators are thought to contribute to ectopic lesion establishment and persistence. Whether circulating immune cells are …

Published: June 4, 2026, midnight
MGST3 Promotes Endometriosis Progression by Suppressing Ferroptosis.

Endometriosis (EMs) is characterized by dysregulated persistence and enhanced invasiveness of ectopic endometrial cells. Current treatment strategies remain limited by high recurrence rates and considerable adverse effects. Although iron overload …

Published: June 3, 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
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
Link copied to clipboard!
Subscribe to Our Newsletter

Stay updated with our latest articles!