Hypoxia and Inflammation
Holger K. Eltzschig, M.D., Ph.D., and Peter Carmeliet, M.D., Ph.D.
N Engl J Med 2011; 364:656-665February 17, 2011
This article has no abstract; the first 100 words appear below.
Mammals have oxygen-sensing mechanisms that help them adapt quickly to hypoxia by increasing respiration, blood flow, and survival responses. If an inadequate supply of oxygen persists, additional mechanisms attempt to restore oxygenation or help the body adapt to hypoxia.1 These other mechanisms rely on oxygen-sensing prolyl hydroxylases (PHDs), which hydroxylate prolines in the alpha subunit of the hypoxia-inducible transcription factor (HIF). This transcription factor is a heterodimer with two subunits: HIF-1α or HIF-2α and HIF-1β (or aryl hydrocarbon receptor nuclear translocator [ARNT] protein). HIF-1α is ubiquitous, whereas HIF-2α is restricted to certain tissues.1
In this review, we show the ways . . .
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From the Department of Anesthesiology, University of Colorado Denver, Aurora (H.K.E.); the Department of Anesthesiology and Intensive Care Medicine, Tübingen University Hospital, Tübingen, Germany (H.K.E.); and Vesalius Research Center VIB, and Vesalius Research Center, K.U. Leuven — both in Leuven, Belgium (P.C.).
Address reprint requests to Dr. Eltzschig at the Department of Anesthesiology, University of Colorado Denver, 12700 E. 19th Ave., Mailstop B112, Research Complex 2, Rm. 7124, Aurora, CO 80045, or at firstname.lastname@example.org.