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MicroRNAs associated with adenomyosis promote endometrial epithelial cell migration via MMP-2 and MMP-9 upregulation†.

Adenomyosis is a common gynecological disorder characterized by the presence of endometrial tissue in the myometrium, causing chronic pelvic pain and abnormal bleeding. Although dysregulated microRNAs (miRNAs) in stromal cells …

Published: Nov. 12, 2025, midnight
Mechanistic Insights into the Anti-Inflammatory and Anti-Proliferative Effects of Selected Medicinal Plants in Endometriosis.

Endometriosis involves oestrogen-dependent chronic inflammation and the abnormal proliferation of ectopic endometrial tissue. Conventional hormonal therapies suppress systemic oestrogen, but do not fully address local oxidative and inflammatory signalling. This …

Published: Nov. 12, 2025, midnight
Lactate-mediated immune suppression and MDSC expansion in endometriosis: Mechanisms and nanoparticle-targeted therapies.

Endometriosis, a chronic gynecological disorder characterized by the ectopic growth of endometrial-like tissue, is associated with severe pelvic pain, infertility, and profound immune dysregulation. Despite advances in hormonal therapy and …

Published: Nov. 1, 2025, midnight
Neuroendocrine-Immune Axis in Endometriosis: A Review on How the Nervous System Goes Beyond Pain Perception.

Endometriosis (EMS) is an estrogen-dependent disorder that affects about 10% of reproductive-age women. EMS affects female neuroendocrine and reproductive functions, greatly compromising female reproductive health and quality of life. However, …

Published: Oct. 31, 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
Reframing Endometriosis: Interplay of NETs, Macrophages, and Lymphocytes at the Crossroads of Disease Progression, Infertility, and Malignant Transformation.

Endometriosis (ENDO) is a painful, chronic gynecological disease widely affecting women globally. While traditionally classified as a hormonal disorder, ENDO is now increasingly recognized as a multifaceted immune-mediated syndrome driven …

Published: Oct. 29, 2025, midnight
A Dual-Targeted Liposomal Nanosystem for Co-Delivery of Estrogen Receptor β Antagonist and Disulfiram for the Non-Hormonal Treatment of Endometriosis.

Endometriosis is an estrogen-dependent disease that severely affects the physical and mental health of women of childbearing age. Due to the significant side effects of traditional hormone therapies, non-hormonal treatment …

Published: Oct. 29, 2025, midnight
Integrated Bioinformatics and Experimental Analysis Revealed Crosstalk Between IL-6, Autophagy, Ubiquitination, and Key miRNAs in Female Infertility: Insights from Ovarian Endometriosis and Polycystic Ovary Syndrome.

Female infertility, affecting millions worldwide, involves complex molecular mechanisms such as chronic inflammation, impaired cellular death, and protein regulation. This study explores how the cytokine IL-6, the autophagy marker LC3, …

Published: Oct. 28, 2025, midnight
Molecular mechanisms and Biological Functions of Autophagy in Endometrial Diseases.

Autophagy is a highly conserved cellular process crucial for maintaining cellular homeostasis by degrading damaged organelles and misfolded proteins. Emerging evidence highlights its pivotal role in endometrial diseases, including endometriosis, …

Published: Oct. 27, 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
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