Gary Fiskum, PhD
The Fiskum lab currently consists of three faculty members, one postdoctoral fellow, a lab manager, a lab helper, one summer medical student, one undergraduate student, three research specialists, and one administrative assistant. Several lab members have been part of the team for over 10 yr. The primary goal of the lab is to improve the understanding of the pathophysiology of both ischemic and traumatic brain injury and relationships between injury to the brain and multiple organ failure. Our approach to this goal utilizes pre-clinical animal models and clinical biomarkers, such as blood cell transcriptomics, bioenergetics, and clinical outcomes in patients with severe brain injury. Our mission is to develop clinically feasible and safe neuroprotective interventions for acute brain injury.
Our lab demonstrated that animals exposed to unnecessary hyperoxia following brain ischemia are 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 greater than 200 peer-reviewed research articles describe the complex interactions between oxidative stress and mitochondrial bioenergetics and the 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. We also 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.
Together with our collaborators at the University of Maryland School of Engineering, we developed a unique model of brain injury caused by explosions targeting military vehicles. Most importantly, modifications of the chassis design reduce brain injury and mortality.
Many brain-injured warfighters are transferred by air within a few days post-injury from combat zones to military medical centers. Using our highly innovative animal models, we demonstrated that the hypobaria experienced during these transfers actually worsens brain injury alone and in combination with polytrauma.
The lab is currently funded by four grants 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.