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The lactate-myeloid-derived suppressor cells axis in endometriosis from molecular reprogramming to translational therapies: A review article.

Endometriosis is a complex chronic condition, driven by estrogen, characterized by the growth of endometrial-like tissue outside the uterus. This often-debilitating disease affects millions of women globally, manifesting as severe …

Published: Sept. 6, 2026, midnight
ATP-P2X3 Signaling as a Shared Neural Sensitization Pathway in Endometriosis and Irritable Bowel Syndrome: Mechanisms and Therapeutic Implications.

Endometriosis and irritable bowel syndrome (IBS) are chronic pain disorders that frequently coexist and share key pathophysiological features, including neuroinflammation, visceral hypersensitivity, peripheral sensitization, and central sensitization. Emerging evidence suggests …

Published: Aug. 25, 2026, midnight
Targeting Imaging Modality in the Diagnosis of Endometriosis: 68Ga-FAPI-04 PET/CT.

Endometriosis is a chronic condition in reproductive-age women, and diagnosis can be delayed for 4-11 years due to nonspecific symptoms and limited imaging. This underscores the need for new methods …

Published: Aug. 24, 2026, midnight
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
Hormonal therapies for endometriosis-associated pain: inflammatory limitations and pharmacological challenges.

Endometriosis is a chronic inflammatory and estrogen-dependent disease in which pain remains the leading cause of impaired quality of life. Hormonal therapies constitute the cornerstone of medical management and include …

Published: Aug. 11, 2026, midnight
NLRP3/Caspase-1-Mediated Pyroptosis Drives a Brain-Lesion Neuroimmune Axis in Endometriosis-Associated Pain: Molecular Mechanisms and Transcranial Direct Current Stimulation Intervention.

Background/Objectives: The NLRP3 inflammasome-Caspase-1-IL-1β pyroptotic axis participates in peripheral inflammatory responses, yet its function in peripheral-central neuroimmune crosstalk underlying endometriosis (EM)-associated pain remains unclear. This study aimed to clarify whether …

Published: July 30, 2026, midnight
Inflammation, Estrogen, and Matrix Remodeling in Female Reproductive Health: From Crosstalk Mechanisms to Translational Diagnostics.

The female reproductive system is a hormonally driven, immune-active, and structurally dynamic system in which estrogen signaling, inflammation, and extracellular matrix (ECM) remodeling interact to support essential reproductive processes. Cyclical …

Published: July 24, 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
The Molecular and Cellular Mechanisms of Melatonin: From Physiological Actions to Clinical Applications in Reproductive Medicine.

Melatonin has evolved from its classical role as a pineal-derived circadian regulator to a molecule increasingly recognized for its mitochondrial and cytoprotective functions. This review examines the molecular mechanisms and …

Published: July 22, 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
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