Placental Extracellular Vesicles Inhibit the Progression of Endometriosis by Inducing Ferroptosis.
Endometriosis (EMs) is an estrogen-dependent chronic inflammatory disease, and its pathogenesis remains unclear. Although the placenta is an organ with tumor-like characteristics, its development, including its invasive function, is tightly …
Reduced type 2 epithelial-mesenchymal transition serves as a risk factor for the progression from endometriosis to endometriosis-associated ovarian cancer.
Endometriosis-associated ovarian cancer (EAOC) is a rare subtype of ovarian cancer arising from the malignant transformation of endometriosis (EMS). Despite growing clinical awareness, its underlying pathogenic mechanisms are not fully …
PRMT3-mediated FOXO1 arginine methylation exacerbates oxidative stress-induced decidualization defects in the eutopic endometrium of endometriosis.
Endometriosis is a hormone dependent disease that often accompanies infertility. At present, the incidence rate of endometriosis is on the rise, but its pathogenesis and the mechanism leading to fertility …
N6-methyladenosine regulated FZD7 inhibits ferroptosis in endometriosis via β-catenin/SLC7A11 pathway.
Endometriosis (EMS), a chronic inflammatory disease affecting approximately 10% reproductive aged women, remains etiologically unclear. This study aims to investigate the role and underlying mechanisms of frizzled class receptor 7 …
Research progress and potential therapeutic targets of a novel disulfide stress-driven cell death-disulfidptosis in gynecological tumors and other gynecological disorders.
Disulfidptosis is a novel Nicotinamide Adenine Dinucleotide Phosphate (NADPH) deficiency-driven cell death pathway characterized by cystine overload and aberrant disulfide bond formation in actin cytoskeletal proteins, distinct from apoptosis, ferroptosis, …