Aberrant epigenetic regulation of estrogen and progesterone signaling at the level of endometrial/endometriotic tissue in the pathomechanism of endometriosis.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic biology without primary clinical data or systematic search methodology.
PubMed 36863794 · doi:10.1016/bs.vh.2022.11.005
What was done
This narrative review synthesized literature on epigenetic regulation of estrogen and progesterone signaling within endometrial stromal cells and mesenchymal stem cells to explain the cellular pathogenesis of endometriosis.
What was found
The abstract reports no numerical findings. It outlines the role of clonogenic endometrial stromal cells with mesenchymal stem cell properties and describes how excess estrogen exposure and progesterone resistance drive epigenetic modifications that contribute to endometriotic lesion development.
Why it matters
It organizes the mechanistic framework linking steroid hormone dysregulation with epigenetic alterations in stem-like endometrial cells during endometriosis establishment.
Limits
As a narrative review, it presents no new clinical or experimental data, includes no quantitative synthesis, and does not specify systematic search methods in the abstract.
Cited by
- supports Endometriosis implants grow in response to estrogen, and their growth slows down in response to progesterone.