New insights into the pathophysiology of endometriosis: from chronic inflammation to danger signal

Hirotaka Kajihara, Kajihara H, Yoshihiko Yamada, Yamada Y, Kanayama S, Seiji Kanayama, Furukawa N, Naoto Furukawa, Noguchi T, Taketoshi Noguchi, Shoji Haruta, Haruta S, Shozo Yoshida, Yoshida S, Sado T, Toshiyuki Sado, Oi H, Hidekazu Oi, Kobayashi H, Hiroshi Kobayashi
Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology · 2010 · vol. 27(2) , pp. 73–79 · doi:10.3109/09513590.2010.507292 · PMID:20712428 · W2061253425
Review OA: closed CC0 ⤵ 69 in-corpus citations
View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-08 ⓘ

This review analyzes gene expression and proteomics studies to explain endometriosis pathophysiology, finding increased markers suggesting sterile inflammation via Toll-like receptor pathways driven by endogenous ligands.

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

Abstract

BACKGROUND: Various theories try to explain the development and progression of endometriosis, however, no single theory can explain all aspects of this disorder. Gene expression profiling studies might reveal factors that explain variability in disease development and progression, which can serve as specific biomarkers for endometriosis and novel drug development. We have recently showed that the upregulated genes were predominantly clustered in stress and detoxification, providing a mechanistic explanation for the oxidative stress and chronic inflammatory response in endometriosis. OBJECTIVE: This review aims: (1) to analyse the published data, with the aim of identifying pathways consistently regulated by the endometriosis genotype and (2) to summarise the findings of specific genes, which are involved in the process of oxidative stress and inflammation. METHODS: We identified gene array and proteomics studies whose data were accessible in PubMed. RESULTS: A major finding is the increased expressions of several markers including heat shock protein, S100, fibronectin, and neutrophil elastase, which might be involved in the process of Toll-like receptor (TLR)-dependent sterile inflammation. The study reviews a convergence in the main pathogenic process, where the TLR-mediated inflammation occurs possibly through the endogenous ligands. CONCLUSIONS: In conclusion, a circulus vitiosus of both the oxidative stress pathway and the TLR pathways is generated when the process becomes chronic (danger signal spiral).

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Endometriosis Inflammation Uterine Diseases Chronic Disease Chronic Disease Disease Progression Disease Progression Endometriosis Endometriosis Endometriosis Endometriosis Female Female Gene Expression Profiling Gene Expression Profiling Humans Humans Inflammation Inflammation Inflammation

Citation neighborhood (2-hop)

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. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (70)

Cited by (50)

Source provenance

europepmc
last seen: 2026-10-17T06:09:56.316927+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-10-08T21:07:58.051504+00:00
unpaywall
last seen: 2026-10-17T06:24:38.187582+00:00
License: CC0 · commercial use OK