Hypoxia and metabolic factors that influence inflammatory bowel disease pathogenesis.
Hypoxia and metabolic factors that influence inflammatory bowel disease pathogenesis.
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DOI：
10.1053/j.gastro.2011.01.056
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发表时间：
2011-05
期刊：
影响因子：
29.4
通讯作者：
Colgan SP
中科院分区：
文献类型：
--
作者：
Glover LE;Colgan SP
胃肠道上皮在解剖位置上提供厌氧管腔和固有层之间的选择性屏障，具有高代谢率。在复杂的脉管系统的支持下，这一重要屏障受到血流量减少和由此导致的组织缺氧的影响，特别是在炎症性肠病（IBD）患者与活动性炎症相关的严重代谢变化期间。在这些条件下，缺氧诱导因子（HIF）的激活促进了疾病小鼠模型中炎症的消退。HIF的保护作用部分归因于肠黏膜屏障保护的复杂调节。通过抑制脯氨酸羟化酶激活HIF的试剂可能会被开发出来，以诱导肠黏膜炎症性疾病患者的缺氧介导的消退。
The gastrointestinal epithelium is anatomically positioned to provide a selective barrier between the anaerobic lumen and lamina propria, which has a high rate of metabolism. Supported by a complex vasculature, this important barrier is affected by reduced blood flow and resultant tissue hypoxia, particularly during the severe metabolic shifts associated with active inflammation in individuals with inflammatory bowel disease (IBD). Activation of hypoxia-inducible factor (HIF) under these conditions promotes resolution of inflammation in mouse models of disease. Protective influences of HIF are attributed, in part, to the complex regulation of a barrier protection with the intestinal mucosa. Reagents that activate HIF, via inhibition of the prolyl hydroxylase enzymes, might be developed to induce hypoxia-mediated resolution in patients with intestinal mucosal inflammatory disease.
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