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炎症性缺氧:缺氧诱导因子的作用

Inflammatory hypoxia: role of hypoxia-inducible factor.

作者信息

Karhausen Jörn, Haase Volker H, Colgan Sean P

机构信息

Center for Experimental Therapeutics and Reperfusion Injury, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.

出版信息

Cell Cycle. 2005 Feb;4(2):256-8. Epub 2005 Mar 1.

Abstract

Sites of inflammation are characterized by significant changes in metabolic activity. Shifts in energy supply and demand can result in diminished delivery and/or availability of oxygen, leading to inflammation-associated tissue hypoxia and metabolic acidosis. These shifts in tissue metabolism, as indicated by previous studies, are frequently associated with vasculitis and profound recruitment of inflammatory cell types, particularly myeloid cells such as neutrophils (PMN) and monocytes. Here, we review recent work addressing the influence of hypoxia on development of inflammatory lesions, with particular emphasis on molecular pathways regulated by hypoxia-inducible factor (HIF).

摘要

炎症部位的特征是代谢活动发生显著变化。能量供需的变化会导致氧气输送减少和/或可用性降低,从而导致与炎症相关的组织缺氧和代谢性酸中毒。如先前研究所表明的,组织代谢的这些变化通常与血管炎以及炎症细胞类型(特别是髓样细胞,如中性粒细胞(PMN)和单核细胞)的大量募集有关。在此,我们综述了近期关于缺氧对炎症性病变发展影响的研究工作,特别强调了由缺氧诱导因子(HIF)调节的分子途径。

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