Jonathan Satin, PhD

Our lab focuses on restoring function to the failing heart and novel mechanisms for developing resilience to a myocardial infarction.  At the cellular and molecular level we focus on the contribution of voltage-gated calcium channel to heart cell physiology.  The  calcium channel in the heart consists of multiple protein-protein interactions. We recently discovered that a protein called Rad is responsible for regulating contractile calcium entry into the myocardium, especially during the fight-or-flight response (promoted by adrenaline stimulated increase in heart function).  One area of research is dedicated to manipulating Rad - channel interactions to increase heart function during the progression of heart failure.  We employ multiple methods included live cell imaging and electrical recordings complemented by in vivo measures of heart function in healthy and disease models.  We also study heart function from an innovative ex vivo heart strip preparation. This allows us to translate findings in cell culture and in mice to large mammals including pigs and human myocardium. A second major area of work studies a novel mammalian regenerative species called Acomys. In collaboration with colleagues in the Department of Biology and at the University of Michigan we are using a variety of techniques such as probing single cell 'transcriptomics' in concert with cellular and animal models to understand how Acomys resists heart damage in response to a myocardial infarction.