Gary Fiskum, PhD
The Fiskum lab currently consists of two faculty members, three postdoctoral fellows, a lab manager, a lab helper, one summer medical student, two undergraduate students, three research specialists, four research assistants and one administrative assistant. The lab focuses on improving the understanding of the pathophysiology of both ischemic and traumatic brain injury, using primarily small animal models. Our mission is to develop clinically feasible and safe neuroprotective interventions for acute brain injury.
Our lab demonstrates that animals exposed to unnecessary hyperoxia following brain ischemia is just as damaging as hypoxia led to a fundamental change in the Advanced Cardiac Life Support Resuscitation guidelines in 2010, a change that has likely improved the survival and quality of life for many thousands of cardiac arrest patients. Many of our 200 peer-reviewed research articles describe the complex interactions between oxidative stress and mitochondrial bioenergetics and development of therapeutic interventions that target these interactions. For example, we were the first to demonstrate that pharmacologic activation of the Nrf2 pathway of antioxidant gene expression protects mitochondria from stress-induced dysfunction. Most recently, we identified sexually dimorphic differences in mitochondrial antioxidant molecules and changes in morphology that may be responsible for the relative resistance of female rat pups to brain injury caused by hypoxia.
The lab is currently funded by one NIH R01 grant and five contracts from either the US Army or US Air Force. We particularly value our collaboration with many other investigators at the University of Maryland Schools of Medicine, Engineering, and Nursing, the Air Force Research Laboratories, and the Walter Reed Army Institute of Research.