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Glycolytic reprogramming in endometriosis: molecular mechanisms, immune modulation, and non-hormonal therapeutic opportunities.

Endometriosis is a chronic gynecological disorder characterized by ectopic tissue growth and significant morbidity, yet current hormonal and surgical treatments often fail to prevent recurrence or entail severe side effects. …

Published: May 25, 2026, midnight
Decidualization potential of endometrial mesenchymal stem cells and their role in reproductive health.

The establishment of a successful pregnancy depends on proper embryo development and coordinated endometrial differentiation, particularly through the process of decidualization. Mesenchymal stem/stromal cells (MSCs), especially those derived from endometrial …

Published: May 23, 2026, midnight
Lesion-centric reprogramming: hydrogel-enabled photothermal reset of endometriosis pain.

Endometriosis-associated pelvic pain represents a prototypical failure of systemic therapy for a locally organized, neuroinflammatory disease. Persistent pain arises from the convergence of estrogen-driven lesion survival, chronic inflammation, fibrosis, and …

Published: May 23, 2026, midnight
Integrative single-cell analysis reveals Bu-Shen-Huo-Xue Formula rescues iron-overloaded ovarian function via rewiring IFN-γ/JAK/STAT/CXCL10-driven immune-stromal interactions and BNIP3-mediated mitophagy in endometriosis.

Ovarian endometriosis (OE) is a leading cause of female infertility. Our previous work identified iron overload-driven oxidative stress and mitochondrial dysfunction in granulosa cells as key pathogenic features, yet the …

Published: May 23, 2026, midnight
Parabacteroides goldsteinii and its metabolite 7-KLCA attenuate endometriosis via TGR5 to reprogram macrophages by modulating the PPARγ/GPR132 axis.

Endometriosis (EMS) remains understudied in effective management strategies. The interplay between macrophage dysfunction and microbiota-derived immune signals emerges as a potential mechanism in EMS pathogenesis, suggesting its relevance for future …

Published: May 22, 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
Extracellular Vesicles in Endometriosis: A Comprehensive Review of Biological Insights and Methodological Challenges.

Endometriosis is a complex disorder associated with dysregulated immune, hormonal, and microenvironmental signaling. Extracellular vesicles (EVs) are important mediators of intercellular communication and may contribute to disease pathogenesis, biomarker discovery, …

Published: May 22, 2026, midnight
ADVANTAGE: Advanced discovery of visceral analgesics by neuroimmune targets and the genetics of extreme human phenotype, a study protocol.

Chronic visceral pain affects over 20% of adults globally but remains poorly understood, significantly impacting quality of life and healthcare costs. Limited understanding and diagnostic misconceptions hinder effective management, particularly …

Published: May 21, 2026, midnight
Luteolin inhibits IL-33/ST2L-induced M2 macrophage polarization in endometriosis.

Endometriosis is a chronic inflammatory disease characterized by immune microenvironment dysregulation, with the IL-33/ST2L signaling axis playing a crucial role in macrophage polarization and disease progression. Despite growing evidence of …

Published: May 21, 2026, midnight
Is Recurrent Endometriosis a Reprogrammed Disease? Molecular Persistence Beyond Surgical Clearance.

Background: Endometriosis is traditionally conceptualized as a localized gynecological disorder characterized by the presence of ectopic endometrial tissue. However, high recurrence rates following apparently complete surgical excision challenge this lesion-based …

Published: May 21, 2026, midnight
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