title: A potential link of oxidative stress and cell cycle regulation for development of endometriosis.
abstract: BACKGROUND
  The roles of molecular alteration such as genomic instability and cell survival are debated aspects of the pathogenesis of endometriosis. To review the contemporary literature on potential factors and their signaling pathways that support prolonged survival of endometriotic cells.
  
  
  METHODS
  This article reviews the English-language literature for molecular, pathogenetic, and pathophysiological studies on endometriosis. This review is focused on the association of hepatocyte nuclear factor (HNF)-1β with endometriosis.
  
  
  RESULTS
  The iron-induced oxidative stress plays a fundamental role for the pathogenesis of endometriosis. Oxidative stress, secondary to influx of iron during retrograde menstruation, modifies lipids and proteins, leading to cell and DNA damage. Recent studies demonstrated HNF-1β overexpression in endometriotic foci. HNF-1β increases the survival of endometriotic cells under iron-induced oxidative stress conditions possibly through the activation of forkhead box (FOX) transcription factors and/or endometriosis-specific expression of microRNAs. Endometriotic cells expressing HNF-1β also display cell cycle checkpoint pathways required to survive DNA damaging events.
  
  
  CONCLUSIONS
  HNF-1β in endometriosis might be a factor that controls the cell cycle and DNA damage checkpoints.
authors.affiliation: Department of Obstetrics and Gynecology, Nara Medical University, Kashihara, Nara, Japan.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Shigetomi
authors.forename: Yumi
authors.initials: Y
authors.lastname: Higashiura
authors.forename: Hirotaka
authors.initials: H
authors.lastname: Kajihara
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kobayashi
mesh_terms: D000818:Animals; D064007:Ataxia Telangiectasia Mutated Proteins; D059447:Cell Cycle Checkpoints; D018797:Cell Cycle Proteins / Q000378:metabolism; D049109:Cell Proliferation; D004249:DNA Damage; D004268:DNA-Binding Proteins / Q000378:metabolism; D004715:Endometriosis / Q000209:etiology* / Q000378:metabolism; D005260:Female; D051858:Forkhead Transcription Factors / Q000378:metabolism; D051539:Hepatocyte Nuclear Factor 1-beta / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D007501:Iron / Q000378:metabolism*; D035683:MicroRNAs / Q000378:metabolism; D018384:Oxidative Stress; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism; D025521:Tumor Suppressor Proteins / Q000378:metabolism
chemical_list: D018797:Cell Cycle Proteins; D004268:DNA-Binding Proteins; D051858:Forkhead Transcription Factors; D035683:MicroRNAs; D025521:Tumor Suppressor Proteins; D051539:Hepatocyte Nuclear Factor 1-beta; D007501:Iron; C576324:ATM protein, human; D064007:Ataxia Telangiectasia Mutated Proteins; D017346:Protein Serine-Threonine Kinases