Targeting HIF-1α to Prevent Renal Ischemia-Reperfusion Injury: Does It Work?

Figure 1

Control of cellular transcription by HIF-α. Under normal oxygen tension, HIF-α is hydroxylated (OH) through an iron (Fe²⁺) dependent pathway to allow recognition by the von Hippel-Lindau (VHL) gene allowing ubiquitination (Ub) and proteosomal degradation. Hydroxylation cannot occur in hypoxia or displacement of iron by metals such as zinc (Zn²⁺), allowing for HIF-α to stabilize and bind with HIF-β within the cell nucleus, resulting in the upregulation of cell survival proteins.