title: The role of iron in the pathogenesis of endometriosis.
abstract: BACKGROUND
  Endometriosis may cause symptoms including chronic pelvic pain and infertility, and increases susceptibility to the development of ovarian cancer. Genomic studies have started to delineate the wide array of mediators involved in the development of endometriosis. Understanding the mechanisms of endometriosis development and elucidating its pathogenesis and pathophysiology are intrinsic to prevention and the search for effective therapies.
  
  
  METHODS
  The present article reviews the English language literature for biological, pathogenetic and pathophysiological studies on endometriosis. Several recent genomic studies are discussed in the context of endometriosis biology.
  
  
  RESULTS
  Severe hemolysis occurring during the development of endometriosis results in high levels of free heme and iron. These compounds oxidatively modify lipids and proteins, leading to cell and DNA damage, and subsequently fibrosis development. Recent studies based on genome-wide expression analysis technology have noted specific expression of heme/iron-dependent mediators in endometriosis. The heme/iron-dependent signaling pathway of endometriosis, which is providing new insights into the regulation of inflammation, detoxification and survival, is discussed.
  
  
  CONCLUSIONS
  Several important endometriosis-specific genes overlap with those known to be regulated by iron. Other genes are involved in oxidative stress. Iron has a significant impact on endometriotic-cell gene expression. This review summarizes recent advances in the heme/iron-mediated signaling and its target genes, outlines the potential challenges to understanding of the pathogenesis and pathophysiology of endometriosis, and proposes a possible novel model.
authors.affiliation: Department of Obstetrics and Gynecology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara, Japan. hirokoba@naramed-u.ac.jp
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kobayashi
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Yamada
authors.forename: Seiji
authors.initials: S
authors.lastname: Kanayama
authors.forename: Naoto
authors.initials: N
authors.lastname: Furukawa
authors.forename: Taketoshi
authors.initials: T
authors.lastname: Noguchi
authors.forename: Shoji
authors.initials: S
authors.lastname: Haruta
authors.forename: Shozo
authors.initials: S
authors.lastname: Yoshida
authors.forename: Mariko
authors.initials: M
authors.lastname: Sakata
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Sado
authors.forename: Hidekazu
authors.initials: H
authors.lastname: Oi
mesh_terms: D004715:Endometriosis / Q000209:etiology* / Q000235:genetics / Q000517:prevention & control / Q000628:therapy; D004717:Endometrium / Q000378:metabolism / Q000473:pathology; D005260:Female; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation; D006418:Heme / Q000235:genetics; D006801:Humans; D007501:Iron / Q000502:physiology*; D010049:Ovarian Diseases / Q000209:etiology* / Q000235:genetics / Q000517:prevention & control / Q000628:therapy
chemical_list: D006418:Heme; D007501:Iron