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首页> 外文期刊>Cellular Signalling >Oxygen homeostasis, thiol equilibrium and redox regulation of signalling transcription factors in the alveolar epithelium [Review]
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Oxygen homeostasis, thiol equilibrium and redox regulation of signalling transcription factors in the alveolar epithelium [Review]

机译：肺泡上皮中的氧稳态，硫醇平衡和信号转导因子的氧化还原调节[综述]

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There is growing evidence linking the pathophysiology of lung disease to an imbalance state of reduction-oxidation (redox) equilibrium. The therapeutic potential of glutathione, an ubiquitous sulfhydryl thiol, and its immunopharmacological properties in the airway epithelium bears clinical consequences for the paediatric treatment of respiratory distress (RD). Dynamic variation in alveolar pO(2) and its effect on redox state may impose a direct role in modulating the pattern of gene expression in lung tissues and, accordingly, could be pivotal in determining cellular fate under these conditions. Hypoxia-inducible factor-1alpha (HIF-1alpha) and nuclear factor-kappaB (NF-kappaB) are redox-sensitive transcription factors of particular importance because their differential activation by reducing and oxidizing signals, respectively, regulate the expression/suppression Of O-2-responsive genes. The regulation of these transcription factors, therefore, which is redox sensitive, is consistent with their roles in coordinating adaptive homeostatic responses to oxidative stress. Functionally, the relationship between 02, glutathione biosynthesis and transcription factor activity bears typical implications for the pattern of cellular survivorship and alveolarization on exposure to O-2-linked stresses. In this review, I discuss (1) the HIF-1alpha/NF-kappaB responsiveness to dynamic changes in pO(2) characteristic of the transition period from placental to pulmonary-based respiration, (2) the capacity of the alveolar epithelium to engage in glutathione biosynthesis and redox shuttling, effectively forming a feedback mechanism governing gene expression, (3) the restitution of antioxidant/prooxidant equilibrium following oxidative challenge and its dependency on the adaptive coordination of responses between redox-associated signalling pathways controlling apoptosis and genetic regulatory factors and (4) a likely association between oxidative stress and the evolution of an inflammatory signal through the pleiotropic O-2-sensitive cytokines. (C) 2002 Elsevier Science Inc. All rights reserved. [References: 76]
机译：越来越多的证据表明，肺部疾病的病理生理与还原-氧化（氧化还原）平衡的不平衡状态有关。谷胱甘肽（一种普遍存在的巯基硫醇）的治疗潜力及其在气道上皮中的免疫药理特性对小儿呼吸窘迫（RD）治疗具有临床意义。肺泡pO（2）的动态变化及其对氧化还原状态的影响可能在调节肺组织中基因表达的模式中起直接作用，因此在确定这些条件下的细胞命运中可能起关键作用。缺氧诱导因子-1α（HIF-1alpha）和核因子-κB（NF-kappaB）是氧化还原敏感的转录因子，因为它们分别通过还原和氧化信号的差异激活来调节O-的表达/抑制，因此它们对氧化还原敏感。 2反应基因。因此，这些转录因子的调节是氧化还原敏感的，与它们在协调对氧化应激的适应性稳态反应中的作用是一致的。在功能上，O 2，谷胱甘肽的生物合成与转录因子活性之间的关系对暴露于O 2连锁压力下的细胞存活和肺泡化模式具有典型意义。在这篇综述中，我讨论了（1）HIF-1alpha / NF-kappaB对pO动态变化的响应性（2）从胎盘呼吸过渡到基于肺的呼吸过渡期的特征，（2）肺泡上皮参与的能力在谷胱甘肽的生物合成和氧化还原穿梭中，有效地形成了控制基因表达的反馈机制，（3）氧化挑战后抗氧化剂/促氧化剂平衡的恢复及其依赖于氧化还原相关信号通路控制细胞凋亡和遗传调控因子之间反应的适应性协调（4）氧化应激与通过多效O-2敏感性细胞因子产生的炎症信号之间可能存在关联。 （C）2002 Elsevier Science Inc.保留所有权利。 [参考：76]

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