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SLC25A1-Mediated Cholesterol Accumulation Promotes Endometriosis Progression by Enhancing Endometrial Stromal Cell Proliferation, Invasion, and M2 Macrophage Polarization.

Endometriosis is an estrogen-dependent chronic inflammatory disorder. Cholesterol (CHO) has been reported to be closely associated with estrogen synthesis and inflammatory responses. Nevertheless, the mechanisms underlying the effects of cholesterol …

Published: Jan. 1, 2026, midnight
UBE2S-mediated deubiquitination of GLUT1 via USP10 regulates glucose metabolic reprogramming and immune microenvironment to promote fibrosis in endometriosis.

Endometriosis (EM) is a chronic inflammatory disorder characterized by the growth of ectopic endometrial-like tissue and fibrosis. Metabolic reprogramming, particularly enhanced glycolysis, and immune microenvironment dysregulation are key features of …

Published: Dec. 5, 2025, midnight
Identification of metabolic reprogramming-associated biomarkers in endometriosis through integrated bioinformatics analysis.

Endometriosis (EMs), a common gynecological disorder, involves complex molecular mechanisms. Metabolic reprogramming (MR) has been recognized as a hallmark of EMs, contributing to lesion survival and immune microenvironment remodeling. This …

Published: Oct. 30, 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
Macrophages in endometriosis: key roles and emerging therapeutic opportunities-a narrative review.

Endometriosis is a chronic gynecological disorder affecting approximately 10% of women of reproductive age. It commonly presents with pelvic pain, dysmenorrhea, and infertility, imposing substantial physical, psychological, and social burdens. …

Published: Oct. 21, 2025, midnight
Activated CD8(+) tissue-resident memory T cells impact the endometrial receptivity in minimal/mild endometriosis.

Endometrial immune disorders create an inhospitable endometrial environment for embryonic nidation in endometriosis. CD8 + tissue resident memory T cells (CD8 +TRM) are abundant tissue resident immune cells in endometrium, …

Published: Oct. 8, 2025, midnight
The dual nature of immunotherapy in female reproductive disorders: immune homeostasis and clinical challenges.

The female reproductive system (FRS) exhibits unique immunological characteristics, balancing defense against pathogens with tolerance to sperm and semi-allogeneic embryos. Key players include decidual natural killer (dNK) cells, immune checkpoint …

Published: Oct. 2, 2025, midnight
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
High-Resolution Spatial Transcriptomics Reveals Fibroblast and Neuroimmune Microenvironments in Endometriosis Lesions.

Endometriosis is a chronic, systemic, inflammatory disease characterized by the presence of endometrium-like tissue growing outside of the uterus. One of its main symptoms is chronic pain and inflammation leading …

Published: Aug. 25, 2025, midnight
Divergent Immune-Metabolic Profiles in Endometriosis and Ovarian Cancer: A Cross-Sectional Analysis.

Endometriosis and high-grade serous ovarian cancer (HGS-OC) share common features within the peritoneal immune microenvironment, yet they exhibit divergent clinical outcomes. This study aimed to dissect the immune-metabolic landscape of …

Published: July 12, 2025, midnight
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