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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
Epigenetics, Oxidative Stress, and the Microbiome in Endometriosis: Toward an Integrated Mechanistic Framework for Precision Medicine.

Endometriosis (EM) is a chronic, estrogen-dependent inflammatory disorder affecting approximately 6-10% of women of reproductive age in the general population and remains a major cause of chronic pelvic pain and …

Published: June 1, 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
From gut-reproductive microbiota to ferroptosis: a comprehensive insight into the molecular-pathogenicity of endometriosis.

Endometriosis (EMS) is a highly heterogeneous chronic gynecological disease characterized by pain, infertility, and relapse, with its etiology and pathogenesis not yet fully elucidated. Traditional theories, including "retrograde menstruation," "implantation …

Published: May 22, 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
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