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Repurposing ramipril to mitigate EMT-like transition in endometriosis by PI3K/AKT/S6K1 signalling pathway: a study in endometriosis induced rats.

Endometriosis, an atypical benign disorder, may disrupt epithelial-mesenchymal transition (EMT) due to a dysregulated balance between matrix metalloproteinases (MMPs) and their inhibitors. Ramipril, an angiotensin converting enzyme (ACE) inhibitor, is …

Published: Jan. 28, 2026, midnight
Hormonal treatment in endometriosis fails to prevent IL-6 increase and endometrium fibrosis but regulates levels of CYP17A, VEGF, and NFkB.

Endometriosis is a gynecological inflammatory disease characterized by the presence of ectopic endometrial-like tissue. This study aims to elucidate the effect of hormonal treatment in human endometriosis inflammation, angiogenesis and …

Published: Jan. 20, 2026, midnight
Eutopic Endometrium Immune Changes Involved in Development and Progression of Endometriosis: A Review.

Numerous abnormalities of the endometriosis eutopic endometrium contribute to the initiation and development of ectopic lesions. It is also believed that among the complex causes of the disease, systemic immunological …

Published: Jan. 8, 2026, midnight
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
THBS1 identificated as an endometriosis biomarker through evidence from single-cell and bulk transcriptomic profiling.

Endometriosis affects a substantial number of women of reproductive age, yet current diagnostic methods rely on invasive procedures. To address this limitation, we investigated THBS1 as a potential biomarker and …

Published: Nov. 21, 2025, midnight
Therapeutic targeting of interleukin-17C signaling in carcinogenesis of endometriosis.

Endometriosis-associated ovarian carcinoma (EAOC) predominantly arises from the malignant transformation of endometriomas, yet the mechanism is incompletely defined. Spatial transcriptomic analysis of human specimens of normal endometrium, endometriomas, and EAOC …

Published: Nov. 20, 2025, midnight
Curcumol alleviates endometriosis via correcting the aberrant activation of Fas/RIPK1-mediated PANoptosis.

Endometriosis (EMs) is an estrogen-dependent chronic inflammatory disease. While apoptosis resistance (evidenced by Bcl-2 upregulation and Bax/caspase-3 downregulation) remains a hallmark of EMs, recent studies reveal a paradoxical coexistence of …

Published: Nov. 18, 2025, midnight
The Interaction of PELP1 With FHL2 Contributes to Ectopic Endometrial Stromal Cell Proliferation, Angiogenesis, and Inflammation in Endometriosis.

Endometriosis (EMS), a multifactorial and chronic benign gynecological disease characterized by ectopic endometrial growth, remains poorly understood in its pathogenesis. Proline, glutamic acid, leucine-rich protein 1 (PELP1), implicated in various …

Published: Oct. 30, 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
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
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