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Protecting the kidney from hypoxia-induced damage

Acute hypoxia-induced often progresses to (CKD), and the progressive loss of kidney function in CKD is linked to (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 , and colleagues at the 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


Journal of Clinical Investigation