UC San Diego

Proper contractile function of the heart requires the balance between energy demand and supply to be constantly maintained. This balance is disrupted by ischemia-reperfusion and leads to cardiac functional defects. Perm1 is a novel protein mainly expressed in skeletal and cardiac muscle and interacts with mitochondrial biogenesis encoding genes. Overexpression of Perm1 reduces cardiomyocyte damage and death following hypoxia-reoxygenation. However, the mechanism of Perm1 function remains unclear. We utilized Perm1 overexpression in transgenic mice to evaluate the alterations in protein expression of various mitochondrial and cellular proteins in response to ischemia-reperfusion. We demonstrated that Perm1 overexpressed hearts did not affect cardiac mass and function at baseline and reduced infarct size upon global ischemia-reperfusion. Further experimentation is needed to verify my results and investigate Perm1 association with other processes of mitochondrial bioenergetics, mitochondrial dynamics, and apoptotic signaling.