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From Endometriosis to Lipedema: Toward a Neuroimmune Framework for Pain Amplification in Hormone-Sensitive Disorders.

Background: Endometriosis and lipedema are chronic female-predominant disorders characterized by persistent pain that is frequently disproportionate to anatomical lesion burden. Although traditionally interpreted within distinct lesion-centered frameworks, both conditions exhibit …

Published: July 3, 2026, midnight
Macrophage-derived exosomes promote proliferation, migration, and invasion of endometrial stromal cells in endometriosis and are associated with exosomal lncRNA ZFAS1: A pilot translational study.

Endometriosis (EMs) is a prevalent gynecological disorder affecting reproductive-age women. Exosomes secreted by peripheral blood macrophages may participate in EMs progression. In this pilot translational study, exosomes from peripheral blood …

Published: June 24, 2026, midnight
Peritoneal Incretin Deficiency and Tirzepatide as a Multi-Axis Adjuvant Hypothesis in Treatment-Refractory Endometriosis: A Mechanistic Framework Linking Metabolism, Immunity, Fibrosis, and Nociception.

Endometriosis is increasingly recognized as a chronic systemic disorder extending beyond the classical estrogen-dependent paradigm, integrating metabolic, immune, fibrotic, and nociceptive pathways that sustain lesion persistence and refractory pelvic pain. …

Published: June 24, 2026, midnight
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
RNF34 restrains endometriosis through SREBP1-dependent metabolic-immune crosstalk.

Endometriosis is a chronic inflammatory disease with cancer-like features, yet the mechanisms linking metabolic dysregulation to immune remodeling during lesion progression remain poorly understood. Here, we identify the ubiquitin E3 …

Published: June 13, 2026, midnight
The role of IL-33/ST2 signaling in female reproductive diseases.

Female reproductive tissues repeatedly undergo controlled inflammation, immune adaptation, and tissue repair. Interleukin-33 (IL-33) and its receptor suppression of tumorigenicity 2 (ST2) sit at the center of these processes, but …

Published: June 12, 2026, midnight
Deciphering immune-inflammatory dysregulation in the endometriotic microenvironment: insights from single-cell omics and artificial intelligence.

Endometriosis is a prevalent chronic inflammatory gynecological disorder affecting approximately 10% of reproductive-age women worldwide, characterized by endometrial-like tissue outside the uterine cavity. Ectopic lesion growth tracks closely with immune-inflammatory …

Published: June 11, 2026, midnight
Endometriosis-associated Pain: Mechanism, Neuroimmune Signature, and Translational Precision Strategies.

Endometriosis affects approximately 10% of reproductive-aged women worldwide and is a leading cause of chronic pelvic pain. Despite its high prevalence and substantial socioeconomic burden, the mechanisms underlying endometriosis-associated pain …

Published: June 10, 2026, midnight
PBMC-derived FGF, PDGF, VEGF and GM-CSF secretion in endometriosis: a case-control in vitro study.

Endometriosis is a chronic inflammatory disease with immune dysregulation in which angiogenic, and hematopoietic mediators are thought to contribute to ectopic lesion establishment and persistence. Whether circulating immune cells are …

Published: June 4, 2026, midnight
Traditional Chinese herbal medicines suppress endometriosis development through modulating macrophage-mediated immune responses in the peritoneal cavity.

Due to unique dietary culture, Asian patients with endometriosis usually seek assistance through traditional Chinese herbal medicine (TCHM), making combined treatments of Western and Chinese medicine quite common in Asia. …

Published: June 1, 2026, midnight
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