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Nat Med. 2000 Dec;6(12):1355-61.

Egr-1, a master switch coordinating upregulation of divergent gene families underlying ischemic stress.

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  • 1Department of Surgery, College of Physicians & Surgeons of Columbia University, 630 West 168th Street, New York, New York 10032, USA.

Erratum in

  • Nat Med 2001 Apr;7(4):509.


Activation of the zinc-finger transcription factor early growth response (Egr)-1, initially linked to developmental processes, is shown here to function as a master switch activated by ischemia to trigger expression of pivotal regulators of inflammation, coagulation and vascular hyperpermeability. Chemokine, adhesion receptor, procoagulant and permeability-related genes are coordinately upregulated by rapid ischemia-mediated activation of Egr-1. Deletion of the gene encoding Egr-1 strikingly diminished expression of these mediators of vascular injury in a murine model of lung ischemia/reperfusion, and enhanced animal survival and organ function. Rapid activation of Egr-1 in response to oxygen deprivation primes the vasculature for dysfunction manifest during reperfusion. These studies define a central and unifying role for Egr-1 activation in the pathogenesis of ischemic tissue damage.

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