Latest Articles

Publication Date
Exploring the Possible Role of Endometriosis-Associated Dysbiosis in Endometrial Carcinogenesis.

Background and Objectives: Endometriosis is associated with chronic inflammation, immune dysregulation, oestrogen-dependent growth, oxidative stress, altered steroid hormone metabolism, compromised epithelial barrier integrity, and the production of bioactive microbial metabolites. …

Published: Aug. 17, 2026, midnight
Integrated lipidomics and transcriptomics reveal the key role of ceramides in the development of endometriosis.

Endometriosis (EMs) is a chronic gynecological disease with poorly understood pathogenesis. This study integrated lipidomics and transcriptomics to systematically investigate aberrant sphingolipid metabolism in EMs, aiming to identify pathogenic mechanisms …

Published: Aug. 11, 2026, midnight
TREM2 Deficiency Attenuates Endometriosis Progression by Inhibiting M2 Polarization of SpMs and Suppressing SIRPα to Enhance Phagocytosis.

Endometriosis (EMS) is characterised by a disrupted peritoneal immune microenvironment where M2 macrophage polarization and impaired phagocytosis promote lesion survival. Single-cell RNA-seq (ScRNAseq) of the peritoneal macrophages from EMS patient …

Published: Aug. 5, 2026, midnight
Recent insights in pathogenesis of endometriosis with focus on gut microbiota.

EMs is a chronic, estrogen-dependent systemic inflammatory disorder defined by the ectopic implantation of endometrial glands and stroma and is frequently associated with dysmenorrhea, chronic pelvic pain, infertility, and substantial …

Published: Aug. 4, 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
Platelet-driven immunothrombotic remodeling programs convert ectopic endometrium into fibrotic, immune-privileged lesions.

Endometriosis is a chronic, heterogenous disorder in which cyclical hemorrhage and repetitive repair generate ectopic implants that persist, recur, and drive pain and infertility; conventional frameworks emphasizing hormonal aberration and …

Published: July 18, 2026, midnight
Targeting the Immune Network in Endometriosis: A Comprehensive Review of Pathogenesis, Immunomodulation, and Emerging Therapies.

Endometriosis is a chronic inflammatory disease characterized by the ectopic growth of endometrial-like tissue and is closely associated with pain and infertility. This review summarizes current evidence on immune dysregulation …

Published: July 12, 2026, midnight
From Endometriosis to Lipedema: Toward a Neuroimmune Framework for Pain Amplification in Hormone-Sensitive Disorders.

Background: Endometriosis and lipedema are chronic female-predominant disorders characterized by persistent pain that is frequently disproportionate to anatomical lesion burden. Although traditionally interpreted within distinct lesion-centered frameworks, both conditions exhibit …

Published: July 3, 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
Deciphering immune-inflammatory dysregulation in the endometriotic microenvironment: insights from single-cell omics and artificial intelligence.

Endometriosis is a prevalent chronic inflammatory gynecological disorder affecting approximately 10% of reproductive-age women worldwide, characterized by endometrial-like tissue outside the uterine cavity. Ectopic lesion growth tracks closely with immune-inflammatory …

Published: June 11, 2026, midnight
Link copied to clipboard!
Subscribe to Our Newsletter

Stay updated with our latest articles!