The laboratory identified that unloading the left ventricle using a percutaneously delivered trans-valvular axial-flow pump) paradoxically increases HIF-1α expression and reduces infarct size during acute myocardial infarction via regulating cardiac metabolism and mitochondrial function in large animal models of ischemia/reperfusion. The current research project in the lab is exploring the role of HIF-1α and its stabilization as a potential therapeutic target for cardioprotective signaling during acute myocardial infarction.
Current projects include:
The Lab identified HIF-1α regulates the cardioprotective signaling with LV unloading before reperfusion hence by reduces infarct size and preserves mitochondrial function during AMI. By employing different kinetics and magnitude of LV unloading prior to reperfusion the lab aims to quantify cardioprotective signaling, calcium homeostasis, energy substrate utilization and ATP production, and mitochondrial integrity.
