缺氧与肺：超越缺氧性肺血管收缩
Hypoxia and the lung: beyond hypoxic vasoconstriction.
作者信息
Nicolls Mark R, Voelkel Norbert F
机构信息
Pulmonary Hypertension Center and Division of Pulmonary and Critical Care Medicine, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA.
出版信息
Antioxid Redox Signal. 2007 Jun;9(6):741-3. doi: 10.1089/ars.2007.1574.
Abstract
This article extends the influence and effects of hypoxia on the lung beyond vasoconstriction and regional blood flow control. Clearly, hypoxia, via the transcription factor hypoxia-inducible factor (HIF)-1alpha, induces a large number of genes encoding proteins, which control cellular metabolism and growth and also participate in inflammation. Hypoxia, likely via vascular endothelial growth factor (VEGF), recruits bone marrow precursor cells to the lung and affects the behavior of immune cells. How hypoxia shapes immune responses through VEGF and its receptors on mast cells, eosinophils, and dendritic cells and through lung endothelial cell/lymphocyte interactions will be a productive area for future research.
摘要
本文将缺氧对肺部的影响扩展至血管收缩和局部血流控制之外。显然，缺氧通过转录因子缺氧诱导因子（HIF）-1α诱导大量编码蛋白质的基因，这些蛋白质控制细胞代谢和生长并参与炎症反应。缺氧可能通过血管内皮生长因子（VEGF）将骨髓前体细胞募集至肺部，并影响免疫细胞的行为。缺氧如何通过VEGF及其在肥大细胞、嗜酸性粒细胞和树突状细胞上的受体以及通过肺内皮细胞/淋巴细胞相互作用来塑造免疫反应，将是未来研究的一个富有成果的领域。
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