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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
RND3 Inhibits Endometriosis Progression by Regulating Autophagy and Oxidative Stress Through PLEKHG5.

Endometriosis (EMS) is a chronic gynecological disease. RND3 is recognized as a potential autophagy-related biomarker in EMS. The aim of this study was to investigate the regulatory role of RND3 …

Published: Oct. 26, 2025, midnight
Ferroptosis in the Ovarian Follicular Microenvironment: A Redox-Dependent Cell Death Pathway with Emerging Roles in PCOS, Oocyte Quality, and IVF Outcomes.

Ferroptosis is a novel kind of regulated cell death that occurs when redox equilibrium is disrupted, leading to iron-dependent lipid peroxidation. Ferroptosis is defined by the buildup of deleterious lipid …

Published: Oct. 25, 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
Correction: Endometrial cancer (EC) derived G3BP1 overexpression and mutant promote EC tumorigenesis and metastasis via SPOP/ERα axis - Cell Communication and Signaling

Correction: Endometrial cancer (EC) derived G3BP1 overexpression and mutant promote EC tumorigenesis and metastasis via SPOP/ERα axis Cell Communication and Signaling

Published: Oct. 24, 2025, 12:50 p.m.
Effects of hormonal treatment on the expression of collagen type I, matrix metalloproteinase-1, and tissue inhibitor of metalloproteinases-1 in endometriosis.

Endometriosis is an estrogen-dependent disease, and hormonal treatment is the most common treatment. Both deep infiltrating endometriosis (DIE) and ovarian endometrioma (OV) are characterized by dense surrounding fibrotic tissue. However, …

Published: Oct. 24, 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
Hypoxia-inducible factor-1 alpha expression in endometriosis: A retrospective observational case-control study of ovarian cyst capsules and endometrial tissue samples.

BackgroundThis study aimed to compare the expression patterns of hypoxia-inducible factor-1α in ovarian cyst capsules and endometrial tissue samples from patients with and without endometriosis to evaluate its potential as …

Published: Oct. 23, 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
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