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再探细胞与分子调节转录机制以及对炎性氧化应激的应答假定途径:当前免疫学突破与概览

On the cellular and molecular regulatory transcriptional mechanisms and responsive putative pathways to inflammatory oxidative stress revisited: current immunological breakthroughs and views at a glance.

作者信息

Haddad John J

机构信息

Department of Medical Laboratory Technology, Faculty of Health Sciences, Beirut Arab University, Beirut, Lebanon.

出版信息

Antiinflamm Antiallergy Agents Med Chem. 2013;12(2):141-57. doi: 10.2174/1871523011312020006.

DOI:10.2174/1871523011312020006
PMID:23363382
Abstract

Responses to oxidative stress are generally regulated by redox-responsive transcription factors (TFs). The abrupt variation in the partial pressure of oxygen (pO2) constitutes a regulatory mechanism. Such TFs forming an integral part of those putative pathways are hypoxia-inducible factor-1α(HIF)-1αand nuclear factor-κB (NF-κB), both are sufficiently tuned to govern such a specific response. Reactive species are produced during this transition and the antioxidant defense system controls their production. Oxidative stress occurs when there is imbalance between the production and removal of reactive species. Evidence exists showing that enhancement of the antioxidant defense system can reduce markers of oxidative stress. Recognition of reactive species and redox-mediated modifications as signals may open up a field of cell regulation via targeted control of TFs and hence can providea novel way of controlling diseases. This synopsis summates the major cutting-edge research work in the field of oxidative stress, and surgically identifies common and unique pathways involved with oxidative stress as means of regulatory elements governing TFs.

摘要

对氧化应激的反应通常由氧化还原反应敏感的转录因子(TFs)调控。氧分压(pO2)的突然变化构成一种调节机制。作为这些假定途径组成部分的此类转录因子包括缺氧诱导因子-1α(HIF)-1α和核因子-κB(NF-κB),二者均能充分调节以控制这种特定反应。在这种转变过程中会产生活性物质,抗氧化防御系统控制它们的产生。当活性物质的产生和清除之间失衡时,就会发生氧化应激。有证据表明,增强抗氧化防御系统可降低氧化应激标志物。将活性物质和氧化还原介导的修饰识别为信号可能会通过对转录因子的靶向控制开辟一个细胞调节领域,从而提供一种控制疾病的新方法。本综述总结了氧化应激领域的主要前沿研究工作,并精准识别了与氧化应激相关的共同和独特途径,作为调控转录因子的调节元件。

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