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Exosomes from miR-149-3p-transfected menstrual blood-derived mesenchymal stem cells ameliorate inflammation and migration of endometriosis cells.

Endometriosis carries remarkable social, public health, and financial consequences. Based on two theories of retrograde menstruation and stem cells, menstrual blood-derived stem cells (MenSCs) play a significant role in endometriosis …

Published: Nov. 1, 2025, midnight
Anti-Angiogenic RNAi-Based Treatment of Endometriosis in a Rat Model Using CXCR4-Targeted Peptide Nanoparticles.

Endometriosis is a common gynecological condition that affects fertility in many women of reproductive age worldwide. This multifaceted disease exhibits a pathogenesis characterized by hormonal and immune system dysregulations, alongside …

Published: Oct. 30, 2025, midnight
Gene Expression Profiling and Pathway Analysis of the Effect of Dienogest on Ovarian Endometriosis: A Comparative Study.

Endometriosis affects about 10% of reproductive-age women and can be managed through medical treatments, surgical intervention, or both. Approximately 40%-50% of patients experience recurrence within 5 years after surgery. Therefore, …

Published: Oct. 29, 2025, midnight
Serum response factor is essential for endometrial function and prevention of inflammatory fibrosis.

Pregnancy requires a supportive uterine environment facilitated by steroid hormone-regulated differentiation of endometrial stromal fibroblasts into decidual cells and tight control of inflammation. Serum response factor (SRF) is a widely …

Published: Oct. 28, 2025, midnight
Integrated bioinformatics analysis and machine learning identifies FZD4, SRPX2, and COL8A1 as angiogenesis hub genes in endometriosis.

This study aims to identify angiogenesis-associated genes (AAGs) in endometriosis (EM) by integrating bioinformatics analysis with machine learning, and to investigate their underlying mechanisms. Differentially expressed genes (DEGs) were screened …

Published: Oct. 26, 2025, midnight
Research progress and potential therapeutic targets of a novel disulfide stress-driven cell death-disulfidptosis in gynecological tumors and other gynecological disorders.

Disulfidptosis is a novel Nicotinamide Adenine Dinucleotide Phosphate (NADPH) deficiency-driven cell death pathway characterized by cystine overload and aberrant disulfide bond formation in actin cytoskeletal proteins, distinct from apoptosis, ferroptosis, …

Published: Oct. 25, 2025, midnight
HMGB-1 Increases Proinflammatory Reaction via TLR4 in Human Granulosa Cells of Endometriosis.

Background/Objectives: Oxidative stress is a critical factor in the development and progression of endometriosis. Granulosa cells, which reside near oocytes in follicles, exhibit steroidogenic activity, and, consequently, influence oocyte quality. …

Published: Oct. 24, 2025, midnight
Identification and Characterization of m6A Regulators METTL3 and YTHDF2: Unveiling Their Biological Functions in Endometriosis.

Endometriosis (EMs) is a benign gynecological disorder that exhibits several malignant characteristics, including proliferation and angiogenesis. N6-methyladenosine (m6A) modification plays a crucial role in regulating RNA splicing, subcellular localization, translation …

Published: Oct. 23, 2025, midnight
Integrative transcriptomic analysis identifies shared EndMT-related gene signatures in endometriosis and recurrent miscarriage.

Endometriosis (EMs) and recurrent miscarriage (RM) represent major reproductive health challenges. This study investigates the involvement of endothelial-mesenchymal transition (EndMT) in these conditions through integrative bioinformatics analysis, focusing on the …

Published: Oct. 21, 2025, midnight
Polychlorinated Biphenyls Alter Estrogen Receptor beta-Mediated Epigenetic Regulation, Promoting Endometriosis.

Endometriosis is a pathological condition characterized by the ectopic growth of endometrial cells, leading to chronic pelvic pain and infertility. Epidemiological studies have associated exposure to dioxin-like polychlorinated biphenyls (PCBs), …

Published: Oct. 7, 2025, midnight
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