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Differential gene expression profiling of ectopic endometrium reveals key molecular pathways in endometriosis pathogenesis.

Endometriosis is a chronic, estrogen-dependent inflammatory disease characterized by the presence of endometrial-like tissue outside the uterine cavity and is associated with pain, infertility, and impaired quality of life. Although …

Published: Feb. 3, 2026, midnight
Influence of Oxidative Stress-Mediated Inflammation on the Pathogenesis of Reproductive Disorders: Exploring the Benefits of Carnosine for Prevention and Treatment of Endometriosis.

Endometriosis is a chronic pathological condition characterized by the growth of endometrial-like tissue outside the uterine cavity and is frequently associated with severe pain, persistent inflammation, and fibrosis within the …

Published: Jan. 30, 2026, midnight
Mucin Biology as a Local Diagnostic and Promising Therapeutic Target in Endometriosis: Expression and Glycosylation Profiling.

Endometriosis (EM) is a chronic inflammatory disease characterized by the growth of endometrial-like tissue outside the uterus, yet its molecular mechanisms remain poorly understood. This study investigated the expression of …

Published: Jan. 20, 2026, midnight
Mechanisms of Luoshi Neiyi prescription (LSNYP) in endometriosis: a network pharmacology and experimental study.

Luoshi Neiyi prescription (LSNYP) is a traditional Chinese medicine that has a clinical effect on endometriosis (EMs). This study combined network pharmacology with experimental validation to explore its potential molecular …

Published: Jan. 19, 2026, midnight
CXCL12 promotes EMT-mediated malignant transformation of endometriosis-associated ovarian cancer via PI3K/Akt signaling: An integrated transcriptomic and clinical study.

Endometriosis-associated ovarian cancer (EAOC) is a distinct form of epithelial ovarian cancer that arises from the malignant transformation of benign endometriotic lesions. While epithelial-mesenchymal transition (EMT) is acknowledged as a …

Published: Jan. 16, 2026, midnight
Network Pharmacology and Multi-omics Investigation of Yiqi Huoxue Formula's Molecular Mechanisms in Treating Endometriosis.

Endometriosis (EMs), a prevalent disorder characterized by pelvic pain and infertility, affects numerous bodily systems and markedly diminishes life quality. Yiqi Huoxue formula (YQHXF) has demonstrated promising therapeutic efficacy. However, …

Published: Jan. 16, 2026, midnight
Aquaporin-9 and Endometriomas: Pathophysiological Insights from a Case-Control Study.

Endometriosis is an estrogen-dependent condition characterized by ectopic implantation of endometrial tissue, yet the molecular mechanisms underlying lesion persistence remain incompletely understood. Aquaporins (AQPs), transmembrane water channels involved in cellular …

Published: Jan. 10, 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
Kisspeptins inhibit ectopic endometrial cell invasion and angiogenesis by suppressing PI3K/AKT signaling pathway via CREB5 in endometriosis.

Endometriosis (EMs) is a common gynecological disorder. According to the most widely recognized theory of retrograde menstruation, endometrial cells require completion of three key steps during ectopic implantation: adhesion, invasion, …

Published: Jan. 1, 2026, midnight
Multi-omics analysis reveals shared diagnostic and therapeutic targets in endometriosis and recurrent implantation failure.

Endometrial receptivity is essential for successful pregnancy, and endometriosis is widely recognized as a disruptor of this process. Poor endometrial receptivity is also a key factor contributing to recurrent implantation …

Published: Dec. 29, 2025, midnight
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