Higher fibrotic content of endometriotic lesions is associated with diminished prostaglandin E2 signaling

Qingqing Huang, Xishi Liu, Sun‐Wei Guo
Reproductive medicine and biology · 2021 · vol. 21(1) , pp. e12423 · doi:10.1002/rmb2.12423 · PMID:34938147 · W3210986517
article OA: gold CC0 ⤵ 20 in-corpus citations
🔓 Open OA copy View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Endometriotic lesions with higher fibrotic content showed reduced COX-2, EP2, and EP4 expression, indicating diminished prostaglandin E2 signaling as fibrosis increases.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

Abstract Purpose While the prevailing view holds that the prostaglandin E2 (PGE 2 ) signaling plays a vital role in endometriosis, PGE 2 also is known to be anti‐fibrotic. We investigated the immunostaining of COX‐2, EP2, and EP4, along with fibrotic content in ovarian endometrioma (OE) and deep endometriosis (DE) lesions, and in OE lesions from adolescent and adult patients. In addition, we evaluated the effect of substrate stiffness on the expression of COX‐2, EP2, and EP4 in endometrial stromal cells. Methods Immunohistochemistry analysis of COX‐2, EP2, and EP4, along with the quantification of lesional fibrosis, was conducted for OE and DE lesion samples and also OE lesion samples from adolescent and adult patients. The effect of substrate rigidity on fibroblast‐to‐myofibroblast transdifferentiation (FMT) and the expression of COX‐2, EP2, and EP4, with or without TGF‐β1 stimulation, were investigated. Results The immunostaining of COX‐2, EP2, and EP4 was substantially reduced in endometriotic lesions as lesions became more fibrotic. Both TGF‐β1 stimulation and stiff substrates induced FMT and reduced the expression of COX‐2, EP2, and EP4. Conclusions Since fibrosis is a common feature of endometriosis, our results thus cast doubts on the use of therapeutics that suppresses the PGE 2 signaling pathway, either by inhibiting COX‐2 or EP2/EP4.

My notes (saved in your browser only)

Condition tags

endometriosisendometrioma

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 (92)

Cited by (20)

Source provenance

europepmc
last seen: 2026-06-04T01:30:01.192114+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:24:03.506079+00:00
License: CC0 · commercial use OK