Activation of hypoxia-inducible transcription factor (HIF) has been identified as an important
mechanism of cellular adaptation to low oxygen. Normoxic degradation of HIF is mediated
by oxygen-dependent hydroxylation of specific prolyl residues of the regulative α-subunits
by HIF prolyl hydroxylases (PHD). It was hypothesized that inhibition of HIF degradation by
either hypoxia or pharmacologic inhibition of PHD would confer protection against
subsequent ischemic injury. For testing this hypothesis ischemic acute renal failure was …