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Interleukin-17A as a key driver for cell migration, proliferation, inflammation, and nerve infiltration in deep endometriosis.

Deep endometriosis (DE) is the most severe subtype of endometriosis, marked by aggressive cellular behavior and debilitating pain. However, the molecular mechanisms underlying DE pathogenesis remain poorly understood. In this …

Published: June 15, 2026, midnight
Anti-NRP1 peptide-engineered ROS/pH dual-responsive nanoparticles for Alpelisib delivery regulate Sema3A-NRP1/PI3K-AKT signaling to balance oxidative stress and inhibit angiogenesis in endometriosis.

Endometriosis progression is driven by oxidative stress and excessive angiogenesis within an inflammatory microenvironment. To overcome these challenges, we designed ROS/pH dual-responsive Alpelisib-loaded nanoparticles (Alp@TAT-AT7-NPs) functionalized with an anti-NRP1 peptide …

Published: June 6, 2026, midnight
Dental pulp-derived mesenchymal stem cells reduce lesion progression in a rat model of endometriosis.

Endometriosis is a chronic, estrogen-dependent inflammatory disease sustained by aberrant angiogenesis and progressive fibrosis. We evaluated the therapeutic efficacy of human dental pulp-derived mesenchymal stem cells (DP-MSCs) in a surgically …

Published: May 30, 2026, midnight
Antagonizing the corticotropin-releasing hormone receptor 1 with an orally bioavailable drug reduces endometriosis pain and associated adhesions†.

Estrogen stimulates corticotropin-releasing hormone (CRH) expression in endometrial tissue, and CRH signaling contributes to inflammation and pain, suggesting a mechanistic role in endometriosis pathophysiology. We previously identified elevated CRH receptor-1 …

Published: May 22, 2026, midnight
Molecular Characterization of Ovarian Endometriosis in Saudi Arabian Women: Insights into Inflammatory, Autophagic, and Epigenetic Dysregulation.

Ovarian endometriosis (OE) is a chronic, inflammatory gynecological disorder associated with sterility and an elevated risk of ovarian cancer. Despite its high prevalence, the complex molecular mechanisms governing OE pathogenesis …

Published: May 20, 2026, midnight
NLRP1 promotes pyroptosis in endometriosis through the NF-κB signaling pathway.

Endometriosis is a prevalent gynecological disorder characterized by chronic inflammation. Pyroptosis, a type of programmed proinflammatory cell death, plays a crucial role in various inflammatory diseases. However, its specific mechanism …

Published: May 14, 2026, midnight
The main active monomer of Dan'e-fukang soft extract, liquiritin, inhibits the inflammation and invasion of ectopic endometrial stromal cells through down-regulation of CCL2.

The study explored the mechanism of Dan'e-fukang soft extract in treating endometriosis (EMs) through network pharmacology. The main active ingredients of Dan'e-fukang soft extract were analyzed based on the traditional …

Published: May 7, 2026, midnight
Curcumin attenuates uterine pain in mice through suppression of neuroinflammation in the DRG and spinal cord.

Uterine pain associated with labor, dysmenorrhea, or endometriosis is often driven by inflammation, which enhances nociceptive signaling and contributes to hyperalgesia. Although nonsteroidal anti-inflammatory drugs (NSAIDs) and glucocorticoids are commonly …

Published: May 6, 2026, midnight
Endometriosis Uncovered: From Chronic Inflammation to Reproductive Dysfunction and Impaired ART Outcomes.

Background and Objectives: Endometriosis is a chronic, estrogen-dependent disorder characterized by the presence of functional endometrial tissue, comprising both glandular and stromal components, located outside the uterine cavity, affecting approximately …

Published: May 5, 2026, midnight
Terazosin as a Non-Hormonal Treatment for Endometriosis.

Endometriosis is a chronic, estrogen-dependent inflammatory disease including aberrant local steroidogenesis, inflammation, angiogenesis, oxidative stress, and prostaglandin-mediated pain. Given the elevated adrenergic receptor expression in endometriotic lesions and the potential …

Published: May 2, 2026, midnight
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