title: New insights into the pathophysiology of endometriosis: from chronic inflammation to danger signal.
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).
authors: Department of Obstetrics and Gynecology, Nara Medical University, Nara, Japan.
authors: Hirotaka
authors: H
authors: Kajihara
authors: Yoshihiko
authors: Y
authors: Yamada
authors: Seiji
authors: S
authors: Kanayama
authors: Naoto
authors: N
authors: Furukawa
authors: Taketoshi
authors: T
authors: Noguchi
authors: Shoji
authors: S
authors: Haruta
authors: Shozo
authors: S
authors: Yoshida
authors: Toshiyuki
authors: T
authors: Sado
authors: Hidekazu
authors: H
authors: Oi
authors: Hiroshi
authors: H
authors: Kobayashi
mesh_terms: D002908:Chronic Disease; D018450:Disease Progression; D004715:Endometriosis / Q000209:etiology* / Q000235:genetics / Q000473:pathology; D005260:Female; D020869:Gene Expression Profiling; D006801:Humans; D007249:Inflammation / Q000150:complications* / Q000235:genetics / Q000473:pathology; D008954:Models, Biological; D015398:Signal Transduction / Q000235:genetics / Q000276:immunology; D051193:Toll-Like Receptors / Q000235:genetics / Q000378:metabolism / Q000502:physiology; D014591:Uterine Diseases / Q000209:etiology* / Q000235:genetics / Q000473:pathology
chemical_list: D051193:Toll-Like Receptors