A potential link of oxidative stress and cell cycle regulation for development of endometriosis
A potential link of oxidative stress and cell cycle regulation for development of endometriosis
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DOI：
10.3109/09513590.2012.683071
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发表时间：
2012-11-01
影响因子：
2
通讯作者：
Kobayashi, Hiroshi
中科院分区：
文献类型：
--
作者：
Shigetomi, Hiroshi;Higashiura, Yumi;Kobayashi, Hiroshi
背景：分子改变的作用，如基因组不稳定性和细胞存活是子宫内膜异位症发病机制中有争议的方面。回顾支持子宫内膜异位症细胞延长存活的潜在因素及其信号通路的当代文献。方法：本文回顾了有关子宫内膜异位症的分子、病理和病理生理研究的英文文献。本文就肝细胞核因子(HNF)-1 β与子宫内膜异位症的关系进行综述。结果：铁诱导的氧化应激在子宫内膜异位症的发病中起重要作用。在月经逆行期间，继发于铁流入的氧化应激改变了脂质和蛋白质，导致细胞和DNA损伤。最近的研究表明，HNF-1 β在子宫内膜异位灶中过表达。HNF-1 β在铁诱导的氧化应激条件下增加子宫内膜异位症细胞的存活率，可能是通过激活叉头盒（FOX）转录因子和/或子宫内膜异位症特异性microrna的表达。表达HNF-1 β的子宫内膜异位症细胞也显示出存活DNA损伤事件所需的细胞周期检查点途径。结论：子宫内膜异位症中的HNF-1 β可能是控制细胞周期和DNA损伤检查点的一个因素
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)-1 beta 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-1 beta overexpression in endometriotic foci. HNF-1 beta 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-1 beta also display cell cycle checkpoint pathways required to survive DNA damaging events. Conclusions: HNF-1 beta in endometriosis might be a factor that controls the cell cycle and DNA damage checkpoints