A potential link of oxidative stress and cell cycle regulation for development of endometriosis

Hiroshi Shigetomi, Yumi Higashiura, Hirotaka Kajihara, Hiroshi Kobayashi
Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology · 2012 · vol. 28(11) , pp. 897–902 · doi:10.3109/09513590.2012.683071 · PMID:22591187 · W2062806267
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This review suggests iron-induced oxidative stress and HNF-1β overexpression are key in endometriosis pathogenesis by promoting endometriotic cell survival and DNA damage checkpoint activation.

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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.

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Condition tags

endometriosis

MeSH descriptors

Cell Cycle Checkpoints Endometriosis Hepatocyte Nuclear Factor 1-beta Iron Oxidative Stress Animals Ataxia Telangiectasia Mutated Proteins Cell Cycle Proteins Cell Cycle Proteins Cell Proliferation DNA-Binding Proteins DNA-Binding Proteins DNA Damage Endometriosis Endometriosis Female Forkhead Transcription Factors Forkhead Transcription Factors Hepatocyte Nuclear Factor 1-beta Humans

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 (61)

Cited by (22)

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