Does hIF-1 reduce ischaemia-reperfusion injury in the heart by targeting the mitochondrial permeability transition pore?
We have demonstrated that acute HIF-1α stabilization using either a pharmacological or genetic approach protected the heart against acute IRI by promoting aerobic glycolysis, decreasing mitochondrial oxidative stress, activating HKII, and inhibiting MPTP opening.
Stratifying CCRCCs according to VHL and VEGF status may help tailor therapeutic strategy.