Taylor Cormac T
UCD Conway Institute, University College Dublin, Belfield, Dublin 4, Ireland.
J Physiol. 2008 Sep 1;586(17):4055-9. doi: 10.1113/jphysiol.2008.157669. Epub 2008 Jul 3.
Decreased oxygen availability (hypoxia) is a hallmark feature of the microenvironment in a number of chronic inflammatory conditions including arthritis and inflammatory bowel disease (IBD). Recent advances in our understanding of oxygen-dependent cell signalling have uncovered several mechanisms by which hypoxia impacts upon the development of inflammation through the coordinated expression of adaptive, inflammatory and apoptotic genes. Two central transcription factors involved in the regulation of this response are hypoxia inducible factor (HIF) and nuclear factor-kappaB (NF-kappaB) which display different degrees of sensitivity to activation during hypoxia. Furthermore, HIF and NF-kappaB demonstrate an intimate interdependence at several mechanistic levels. Recent studies indicate that these pathways may represent important new therapeutic targets in diseases characterized by hypoxic inflammation.
氧气供应减少（缺氧）是包括关节炎和炎症性肠病（IBD）在内的多种慢性炎症性疾病微环境的一个标志性特征。我们对氧依赖性细胞信号传导的理解最近取得的进展揭示了几种机制，通过这些机制，缺氧通过适应性、炎症性和凋亡基因的协调表达影响炎症的发展。参与这种反应调节的两个核心转录因子是缺氧诱导因子（HIF）和核因子-κB（NF-κB），它们在缺氧期间对激活表现出不同程度的敏感性。此外，HIF和NF-κB在几个机制层面上表现出密切的相互依赖性。最近的研究表明，这些途径可能是缺氧性炎症相关疾病重要的新治疗靶点。
