The overall goal of Dr. Sharp’s research is to understand the fundamental mechanisms that couple mitochondrial behavior with cellular energetic demand. Specifically, his lab studies how substrate limitations or increased workload of the cell are coupled with altered mitochondrial metabolism, dynamics, and biogenesis to meet these demands. These cellular principles have particular translational relevance in the setting of cardiac arrest, myocardial infarction, sepsis, and traumatic injury.

Dr. Sharp is also investigating the protective effects of mild hypothermia at the cellular and tissue level. Hypothermia is used during cardiac surgery, has been shown to improve outcomes from cardiac arrest in randomized clinical trials. While hypothermia is known to slow the utilization of ATP, Dr. Sharp’s lab has demonstrated that hypothermia also appears to specifically block known signaling pathways that regulate the mitochondria including AMPK and mTOR. Recent work by the lab also demonstrates that hypothermia regulates DRP1, a known modulator of mitochondrial fission and metabolism. Since hypothermia is one of the few clinically proven tools used to improve patient outcomes, understanding its effects on mitochondrial behavior could lead to improved pharmacological strategies for treating patients. Dr. Sharp’s work through its basic science and translational approaches has the potential for high impact discovery.