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SPP1 as a key modulator of M2 macrophage polarization promotes endometriosis progression via activation of the FAK/PI3K/AKT pathway: A bioinformatics and experimental study.

Endometriosis (EMs) is a gynecological disorder characterized by chronic inflammation and an aberrant immune microenvironment. In this study, we integrated the GSE6364 dataset from the GEO database to identify differentially …

Published: Sept. 17, 2025, midnight
Integrated GNPS, semi-preparative HPLC, and network pharmacology reveal active ingredients and potential machenisms of Paeonia suffruticosa Andr. leaves in treating endometriosis with anxiety/depression.

Endometriosis (EMs) with anxiety/depression is a common comorbidity of EMs, yet effective treatments are still lacking. Leaves of Paeonia suffruticosa Andr. (PSL) have potential therapeutic effects on EMs and their …

Published: Sept. 15, 2025, midnight
Helixor A enhances natural killer cell activity by induction of PAI-1 expression through the p38/MAPK signaling pathway.

Helixor A, an anticancer drug, has an immunostimulatory effect that increases T and natural killer (NK) cell activity in patients with cancer and endometriosis. However, the molecular mechanisms underlying its …

Published: Sept. 12, 2025, midnight
Polychlorinated biphenyl Endocrine Disruptor Alters Estrogen Receptor beta-Mediated Epigenetic Regulation, Promoting Endometriosis.

Background Endometriosis is a pathological condition characterized by the ectopic proliferation of endometrial cells, resulting in chronic pelvic pain and infertility. Exposure to endocrine-disrupting chemicals (EDCs) has been implicated in …

Published: Sept. 4, 2025, midnight
Neuroinflammation is responsible for pain in endometriosis - targeting the JAK-STAT pathway and mast cell activation.

Chronic pain is a defining feature of endometriosis and contributes significantly to the diminished quality of life observed in affected individuals. Despite advances in understanding disease pathology, current therapeutic strategies …

Published: Aug. 29, 2025, midnight
Elucidation of the mechanism of treating endometriosis with Ge Xia-Zhu Yu decoction by means of network pharmacology and molecular docking.

This study investigates the mechanism of Ge Xia-Zhu Yu decoction (GXZYT) in the treatment of endometriosis (EMS). The active components and targets of GXZYT were screened using TCMSP database and …

Published: Aug. 27, 2025, midnight
Expression profiles of E-cadherin and N-cadherin in endometriosis and other gynecological diseases towards targeted treatment: a systematic review.

This systematic review aimed to summarize all available data and evaluate the roles of E-cadherin, N-cadherin, associated molecules, and signaling pathways in the pathogenesis of endometriosis. The search was conducted …

Published: Aug. 21, 2025, midnight
EETs Reduction Contributes to Granulosa Cell Senescence and Endometriosis-Associated Infertility via the PI3K/AKT/mTOR Signaling Pathway.

We aimed to examine abnormal oxidative lipid levels and their related mechanisms in EM-associated infertility. Through liquid chromatography tandem mass spectrometry analysis, decreased levels of epoxyeicosatrienoic acids (EETs), which have …

Published: Aug. 19, 2025, midnight
Effects of Mono- (2-ethylhexyl) phthalate and Phthalic Acid Monobenzyl Ester on endometriosis using network toxicology, machine learning and molecular docking techniques.

Phthalate metabolites Mono- (2-ethylhexyl) phthalate(MEHP) and Phthalic Acid Monobenzyl Ester (MBZP) are widely present in the environment, can interfere with the endocrine system and accumulate in human tissues, and are …

Published: Aug. 8, 2025, midnight
Insights into the Molecular Mechanisms and Signaling Pathways of Epithelial to Mesenchymal Transition (EMT) in the Pathophysiology of Endometriosis.

Endometriosis is a disease characterized by the presence of endometrial glands and stroma outside of the uterine corpus, often clinically presenting with pain and/or infertility. Ectopic lesions exhibit features characteristic …

Published: Aug. 1, 2025, midnight
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