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The role of insulin-like growth factor binding proteins in TGF-β1-induced fibroblast-myofibroblast transition during endometriosis fibrosis.

Fibrosis is a defining feature of endometriosis (EMS). Our previous single-cell RNA sequencing (scRNA-seq) revealed myofibroblasts (MFBs) as the predominant cells in ectopic endometrium (ECE), mainly derived from fibroblast-to-myofibroblast transition …

Published: Jan. 9, 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
Navigating Complexity: Review and Updates of Endometriosis and Adenomyosis Imaging.

Endometriosis and adenomyosis are prevalent chronic inflammatory conditions that significantly impact reproductive-age women, leading to debilitating symptoms such as pelvic pain, dysmenorrhea, and infertility. Endometriosis is characterized by ectopic endometrial …

Published: Jan. 8, 2026, midnight
Ginsenoside Rg3 antagonises endometriosis glycolysis via the tripartite motif containing 28 and pyruvate dehydrogenase kinase 4 signalling pathway.

Endometriosis is a common gynaecological disorder characterised by the ectopic growth of endometrial-like tissue, which can lead to clinical symptoms such as chronic inflammation, pelvic pain, and infertility. Aberrant cellular …

Published: Jan. 7, 2026, midnight
The diagnosis of postcesarean delivery complications with imaging techniques (ultrasound, computed tomography, magnetic resonance imaging, X-ray, and angiography).

Cesarean delivery, one of the most common surgeries performed worldwide, carries the risk of complications. These complications affect both mothers and newborns, but in this review, only maternal complications will …

Published: Jan. 6, 2026, midnight
Evidence for KISS-1 nuclear translocation and PI3K/AKT signaling in the ultrastructurally and morphometrically analyzed human endometriosis.

Endometriosis is a common estrogen-dependent disease marked by ectopic endometrial growth. Although the PI3K/AKT and kisspeptin pathways are known to regulate endometrial homeostasis, their interplay in disease progression remains unclear. …

Published: Jan. 6, 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
Vaginal Contraception With NuvaRing Decreases Symptoms and Uterine Features of Adenomyosis: A Prospective Evaluation.

(Abstracted from Contraception 2025:150:111016, doi:10.1016/j.contraception.2025.111016) Adenomyosis occurs when ectopic endometrial glands invade the myometrium and can cause symptoms such as an enlarged uterus, heavy menstrual bleeding, pelvic pain, infertility, and …

Published: Dec. 31, 2025, midnight
Tellimagrandin II Stimulates Inflammasomes by Causing an Accumulation of 3-Aminopropanal, Which Promotes Apoptosis of Endometriotic Cells While Inhibiting Invasion.

Endometriosis is frequently treated with Paeoniae Radix. It contains Tellimagrandin II, which has the role of modulating immunity and anti-tumor. Therefore, we will explore the effects of Tellimagrandin II on …

Published: Dec. 29, 2025, midnight
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