Cardioprotective HIF-1α-frataxin signaling

 

Previous studies have demonstrated the protective signaling of Hypoxia Inducible Factor -1 alpha (HIF-1α) against ischemia/ reperfusion (IR) injury in the heart. In this study, we provide further evidence for a cardioprotective mechanism by HIF-1α against IR injury exerted via the mitochondrial protein frataxin, which regulates mitochondrial iron-sulfur (Fe-S) cluster formation. The disruption of frataxin has been found to induce mitochondrial iron overload and subsequent reactive oxygen species (ROS) production. We observed that frataxin expression is elevated in mice hearts subjected to IR injury, and this response was blunted in cardiac specific HIF-1α knockout (KO) mice.