Commentary: Somatic Stem Cells and Their Dysfunction in Endometriosis
This commentary discusses the role of somatic stem cell dysfunction in the pathogenesis of endometriosis, exploring potential therapeutic targets for disease management.
One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works
This commentary reviews somatic stem cells—particularly endometrial stem cells—and how their dysfunction may contribute to endometriosis pathogenesis, discussing high-level mechanisms such as EMT/MET, stem cell niches, menstrual-effluent–induced signaling, and the potential contribution of bone marrow–derived stem cells. The authors highlight evidence that EMT/MET-like processes and EMT activity in side population cells could facilitate migration, invasion, and ectopic lesion establishment, and they cite studies linking miR-200b and ZEB1/2/KLF4 to EMT, invasiveness, and stemness. A key limitation is that the piece is a narrative commentary compiling findings from multiple studies rather than presenting new experimental data, and it frames many connections as associations requiring further investigation. This paper is centrally about endometriosis — it synthesizes literature on somatic/endometrial stem cells and their dysregulation in relation to EMT/MET and the stem-cell niche in endometriosis.
Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works
Abstract
Full text
11,529 characters
· extracted from
oa-doi-fallback
· 2 sections
· click to expand
References
Keywords
Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.
My notes (saved in your browser only)
Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works
Condition tags
Citation neighborhood
Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.
References (11)
- Contribution of Bone Marrow-Derived Stem Cells to Endometrium and Endometriosis via openalex
- Human Endometrial Fibroblasts Derived from Mesenchymal Progenitors Inherit Progesterone Resistance and Acquire an Inflammatory Phenotype in the Endometrial Niche in Endometriosis1 via openalex
- microRNA miR-200b affects proliferation, invasiveness and stemness of endometriotic cells by targeting ZEB1, ZEB2 and KLF4 via openalex
- Proteome analysis of human mesothelial cells during epithelial to mesenchymal transitions induced by shed menstrual effluent via openalex
- Somatic Stem Cells and Their Dysfunction in Endometriosis via openalex
- Treatment of Endometriosis via openalex
- W2171875732 via openalex
- W2104952524 via openalex
- W2322133447 via openalex
- W2036591541 via openalex
- W2029141740 via openalex
Cited by (3)
Source provenance
- europepmc
- last seen: 2026-06-12T06:13:51.797165+00:00
- openalex
- last seen: 2026-06-10T17:14:06.276822+00:00
- pubmed
- last seen: 2026-05-13T22:20:19.560968+00:00