Pathogenesis of endometriosis — Current research

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AI-generated summary by claude@2026-06, 2026-06-08

Endometrial cells adhere to and invade peritoneal mesothelium rapidly, indicating mesothelial surface molecules, potentially CD44-hyaluronan binding, are key to endometriosis pathogenesis.

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Abstract

Proliferative, secretory and menstrual endometrial cells of both the stroma and epithelium adhere to intact peritoneal mesothelium and mesothelial monolayers. Endometrial attachment to the mesothelium appears to occur rapidly (within 1 h) and transmesothelial invasion occurs between 1 and 18-24 h. These results demonstrate that the mesothelium is not a 'no-stick' surface and indicates that molecules present at the surface of the mesothelium are involved in the pathogenesis of the early endometriotic lesion. The inhibition of endometrial cell adherence to peritoneal mesothelium by hyaluronidase indicates that CD44-hyaluronan binding is at least one of the mechanisms involved in the pathogenesis of endometriosis. We believe that investigation of mesothelial cell adhesion molecules is central to understanding the pathogenesis of endometriosis.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Endometriosis Cell Adhesion Endometriosis Endometriosis Epithelial Cells Epithelial Cells Epithelium Epithelium Female Humans Hyaluronan Receptors Hyaluronan Receptors Hyaluronic Acid Hyaluronic Acid Hyaluronoglucosaminidase Hyaluronoglucosaminidase Menstruation Peritoneum Peritoneum Stromal Cells

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 (22)

Cited by (13)

Source provenance

europepmc
last seen: 2026-06-04T01:30:01.192114+00:00
openalex
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