The Molecular and Cellular Mechanisms of Endometriosis: From Basic Pathophysiology to Clinical Implications.
Level 5 - mechanism / opinion, no new human data
Narrative review of molecular mechanisms and pathophysiology without systematic search or original human data.
PubMed 40141102 · doi:10.3390/ijms26062458
What was done
The authors reviewed literature on the genetic, epigenetic, immune, and molecular mechanisms governing endometriosis development, ectopic lesion survival, and related therapeutic strategies.
What was found
The abstract provides no quantitative data or numerical findings. It outlines that lesion establishment involves endometrial mesenchymal stem cells and epithelial progenitors, aberrant signaling via PI3K/Akt and Wnt/β-catenin, elevated estrogen, and progesterone resistance. Immune dysfunction—specifically altered macrophage activity and impaired natural killer cell function—enables lesion persistence, while prostaglandin E2 and nerve infiltration drive pain.
Why it matters
Mapping the cellular pathways and immune mechanisms involved in endometriosis highlights alternative targets for personalized therapies beyond conventional hormonal suppression.
Limits
The abstract describes a broad narrative synthesis without systematic search methodology, quality assessment of cited studies, or primary human trial data.
Cited by
- supports Endometriosis implants grow in response to estrogen, and their growth slows down in response to progesterone.