Iron-Dependent Oxidative Stress as a Pathogenesis for Preterm Birth
Iron-Dependent Oxidative Stress as a Pathogenesis for Preterm Birth
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DOI：
10.1097/ogx.0b013e318181a79f
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发表时间：
2008-10
影响因子：
6.2
通讯作者：
M. Sakata;T. Sado;Takashi Kitanaka;K. Naruse;T. Noguchi;S. Yoshida;H. Shigetomi;A. Onogi;H. Oi;Hiroshi Kobayashi
中科院分区：
文献类型：
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作者：
M. Sakata;T. Sado;Takashi Kitanaka;K. Naruse;T. Noguchi;S. Yoshida;H. Shigetomi;A. Onogi;H. Oi;Hiroshi Kobayashi
问题：早产（PTB）是一种氧化应激相关的疾病，缺乏有效的治疗方法，部分原因是对疾病的发病机制认识不足。这篇文章的目的是回顾可能导致PTB发病机制的分子途径。基因组学和蛋白质组学研究已经开始描绘广泛的介质参与这种疾病。了解PTB的发展机制，阐明发病机制和病理生理学是预防和有效治疗这种疾病的内在因素。研究方法。本文综述了PTB发病机制和病理生理学研究的英文文献。最近的几个基因组和蛋白质组学研究的PTB生物学的背景下进行了讨论。结果如下：在PTB患者的胎盘中，组织学上已经确定了蜕膜出血，这可能导致高水平的游离血红素和铁。几个重要的PTB特异性基因和蛋白质与那些已知由铁调节的基因和蛋白质重叠。其他的是与氧化应激和解毒有关的基因。游离铁氧化修饰脂质和蛋白质，导致DNA和细胞损伤。PTB的信号通路将被讨论，因为它为炎症，氧化应激和解毒的调节提供了新的见解。结论：本文综述了血红素/铁介导的信号转导及其靶基因的研究进展，并对PTB发病机制和病理生理学的理解提出了挑战。提出了一种新的模型。总的来说，蜕膜出血和炎症被认为是PTB发病机制的主要贡献者。目标受众：妇产科医师，家庭医生学习目标：完成本文后，读者应该能够解释氧化应激在早产发病机制中的作用，解释早产作为一种“综合征”的概念，并总结早期子宫出血在早产病理生理学中的潜在作用。
Problem: Preterm birth (PTB) is an oxidative stress-related disease that lacks effective therapies partly because of the poor understanding of disease pathogenesis. The aim of this manuscript was to review molecular pathways that could be responsible for the pathogenesis of PTB. Genomic and proteomic studies have started to delineate the wide array of mediators involved in this disorder. Understanding the mechanisms of the development of PTB and elucidating pathogenesis and pathophysiology are intrinsic to prevention and effective therapies for this disorder. Method of Study. This article reviews the English language literature for pathogenesis and pathophysiological studies on PTB. Several recent genomic and proteomic studies are discussed in the context of PTB biology. Results: Decidual hemorrhage has been identified histologically in the placentas of patients with PTB, which may result in high levels of free heme and iron. Several important PTB-specific genes and proteins overlap with those known to be regulated by iron. Others were genes involved in oxidative stress and detoxification. Free iron oxidatively modifies lipid and protein, leading to DNA and cell damage. This signaling pathway of PTB will be discussed as it provides new insights into regulation of inflammation, oxidative stress, and detoxification. Conclusion: This review summarizes recent advances in heme/iron-mediated signaling, the target genes thereof, and the potential challenges to the understanding of pathogenesis and pathophysiology of PTB. A novel model is proposed. Collectively, decidual hemorrhage and inflammation are considered to be major contributors to the pathogenesis of PTB. Target Audience: Obstetricians & Gynecologists, Family Physicians Learning Objectives: After completion of this article, the reader should be able to paraphrase the role of oxidative stress in pathogenesis of preterm birth, explain the idea of preterm birth as a “syndrome,” and summarize the potential role of early uterine bleeding in pathophysiology of preterm birth.