Latest Articles

Publication Date
Parabacteroides goldsteinii and its metabolite 7-KLCA attenuate endometriosis via TGR5 to reprogram macrophages by modulating the PPARγ/GPR132 axis.

Endometriosis (EMS) remains understudied in effective management strategies. The interplay between macrophage dysfunction and microbiota-derived immune signals emerges as a potential mechanism in EMS pathogenesis, suggesting its relevance for future …

Published: May 22, 2026, midnight
Luteolin inhibits IL-33/ST2L-induced M2 macrophage polarization in endometriosis.

Endometriosis is a chronic inflammatory disease characterized by immune microenvironment dysregulation, with the IL-33/ST2L signaling axis playing a crucial role in macrophage polarization and disease progression. Despite growing evidence of …

Published: May 21, 2026, midnight
ASPM promotes the progression of ovarian endometriosis by modulating the cell cycle and activating the Wnt/β-catenin signaling pathway.

Endometriosis (EMs) is a common gynecological disorder associated with impaired fertility and reduced quality of life. This study investigated abnormal spindle-like microcephaly-associated protein (ASPM), identified as a hub gene in …

Published: May 20, 2026, midnight
Hypoxia-mediated epigenetic silencing of YTHDF2 promotes endometriosis progression via the NFE2L1-NF-κB axis.

Endometriosis (EMs) is a chronic inflammatory disease characterized by ectopic growth of endometrial-like tissues. N6-methyladenosine (m6A) modification regulates diverse cellular processes, yet its role in EMs remains unclear. Here, we …

Published: May 19, 2026, midnight
Single-cell profiling and machine learning identify cuproptosis-related fibroblast subpopulations and fibrogenesis modulator AEBP1 in endometriosis.

Endometriosis is characterized by progressive fibrosis and limited therapeutic options. Cuproptosis, a copper-dependent form of regulated cell death, has been implicated in multiple pathological conditions, but its relevance to fibroblast-mediated …

Published: May 18, 2026, midnight
HSD11B1 suppresses ferroptosis in endometrial stromal cells through the JUND/IL-10 axis to promote endometriosis progression.

Endometriosis (EMs) is a common gynecological disorder characterized by ectopic endometrial tissue growth, leading to chronic inflammation and pelvic pain. Despite its high prevalence, the molecular mechanisms underlying EMs remain …

Published: May 18, 2026, midnight
Nuclear factor IX promotes endometriosis progression through transcriptional activation of tetraspanin-2.

Endometriosis is a benign yet aggressive disease characterized by enhanced proliferation and invasion of ectopic endometrial tissue. Identifying upstream regulators that co-regulate these processes will provide novel insights into endometriosis …

Published: May 16, 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 role of the SIRT1/FOXO1 axis in regulating autophagy and inflammation in endometriosis.

Endometriosis, a common chronic gynecological disorder, involves cellular autophagy and inflammatory processes in its pathogenesis. However, the specific regulatory mechanisms of autophagy and inflammation in endometriosis remain unknown. In this …

Published: May 13, 2026, midnight
Glycolytic reprogramming and MYH10 K1520 lactylation mediate eutopic endometrial collagen I deposition driven by PKM2-packaged ectopic endometrial extracellular vesicles.

Endometriosis (EMs) is characterized by ectopic lesions that disrupt endometrial decidualization, a process frequently accompanied by aberrant collagen deposition and closely linked to clinical infertility. Extracellular vesicles (EVs) are key …

Published: May 11, 2026, midnight
Link copied to clipboard!
Subscribe to Our Newsletter

Stay updated with our latest articles!