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JCI online ahead of print table of contents for May 1, 2014
Date:5/1/2014

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Marco Mongillo
Venetian Institute of Molecular Medicine, Padova, UNK, ITA
Phone: 390497923229; Fax: 390497923250, E-mail: marco.mongillo@unipd.i

View this article at: http://www.jci.org/articles/view/66339


Protecting the kidney from hypoxia-induced damage

Acute hypoxia-induced renal injury often progresses to chronic kidney disease (CKD), and the progressive loss of kidney function in CKD is linked to endothelial cell (EC) damage. The hypoxia-inducible transcription factors HIF-1 and HIF-2 are expressed in renal ECs following ischemic injury, but the specific contributions of these mediators to pathogenesis are not clear. In this issue of the Journal of Clinical Investigation, Volker Haase and colleagues at the Vanderbilt University School of Medicine used murine models of hypoxic kidney injury, to evaluate the contribution of endothelial HIF-1 and HIF-2 toward the development of ischemia-induced pathogenesis. Loss of HIF-2 alone markedly increased kidney inflammation and fibrosis following ischemic injury and was associated with increased expression of the neutrophil adhesion molecule VCAM1. Blocking VCAM1 in HIF-2-deficient mice reduced hypoxia-associated phenotypes. Furthermore, enhancing HIF-2 activation in WT mice prior to ischemia and reperfusion protected animals from kidney injury. Together, these data indicate that endothelial HIF-2 protects kidney from hypoxia-induced damage.

TITLE: Endothelial HIF-2 mediates protection and recovery from ischemic kidney injury

AUTHOR CONTACT: Volker Hans Haase
Vanderbilt University, Nashville, TN, USA
Phone: 615 343-7254; Fax: 615 322-6854; E-mail: volker.haase@vanderbilt.edu

View this article at:

Contact: Corinne Williams
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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