Dysfunction of natural killer cells promotes immune escape and disease progression in endometriosis Frontiers
The involvement of lncRNA EMSLR in the disulfidptosis and progression of endometrial carcinoma Nature
Endometriosis is a chronic, estrogen-dependent condition affecting over 190 million women globally, characterized by the ectopic presence of endometrial-like tissue that leads to inflammation, pain, and infertility. Despite its prevalence, …
Through a combination of single-cell/single-nucleus RNA-sequencing (sc/snRNA-seq) data analysis, immunohistochemistry, and primary macrophage studies, we have identified pathogenic macrophages characterized by TET3 overexpression (Toe-Macs) in three major human diseases associated …
Single-cell sequencing uncovers disrupted stromal-macrophage communication as a driver of intrauterine adhesion progression Nature
Endometriosis, a chronic estrogen-dependent disorder defined by ectopic endometrial-like tissue growth, causes pelvic pain and infertility in reproductive-age women. Despite its prevalence, the underlying mechanisms driving lesion persistence and reproductive …
Endometriosis (EMS) is a prevalent estrogen-dependent gynecological disorder characterized by ectopic growth of endometrial tissue. Central to its pathophysiology, peritoneal CD14hi macrophages exhibit a pro-EMS phenotype and drive disease progression. …
To evaluate the progression of endometriosis and painful symptoms in young women (≤ 25 years) with severe dysmenorrhea (Visual Analogue Scale score ≥ 7), with or without ultrasound-detected endometriosis, over …
Endometriosis is a chronic, estrogen-dependent disorder characterized by the ectopic growth of endometrial-like tissue. Despite its significant impact on fertility and quality of life, the pathogenesis of endometriosis remains poorly …
Endometriomas affect up to 44% of women with endometriosis and are associated with chronic pelvic pain, infertility, and reduced ovarian reserve. Diagnosis and management are clinically challenging, requiring a nuanced …