Marschall Runge has served as executive vice president for medical affairs since March 2015.

Before joining the University of Michigan, he was executive dean for the University of North Carolina School of Medicine, the Charles Addison and Elizabeth Ann Sanders distinguished professor of medicine at UNC-Chapel Hill, chair of the UNC-CH Department of Medicine, and principal investigator and director of the NIH-funded North Carolina Translational and Clinical Sciences Institute, one of 55 medical research institutions working together as a national consortium to improve the way biomedical research is conducted across the country.

An honors graduate of Vanderbilt University with a bachelor of arts degree in biology and a Ph.D. in molecular biology, he earned his M.D. from the Johns Hopkins School of Medicine, where he was an intern and resident in internal medicine. He completed a cardiology fellowship at Harvard’s Massachusetts General Hospital and was a faculty member there prior to moving to Emory University as an associate professor of medicine in 1989. Before joining the UNC faculty in 2000, he held the John Sealy Distinguished Centennial Chair in Internal Medicine and was director of the Division of Cardiology and the Sealy Center for Molecular Cardiology at the University of Texas Medical Branch at Galveston.

He holds five patents and is a past president of the American Heart Association, Galveston Island Division, and the Paul Dudley White Society at Massachusetts General Hospital.

One of the major focuses of my research has been studying the role of mitochondrial oxidative stress in the pathogenesis of cardiovascular disease. Our lab was one of the first to provide experimental evidence that mitochondrial DNA damage is not only correlated with atherosclerotic lesions in human aortic tissue and aortas from Apoe-/- mice but also preceded atherogenesis in young Apoe-/- mice. Apoe-/- mice deficient in mitochondrial antioxidant enzyme Sod2 (Apoe-/- /Sod2+/-) exhibit early increases in mitochondrial DNA damage and a phenotype of accelerated atherogenesis at the arterial branch point. Furthermore, we showed that Sod2 deficiency increases endothelial dysfunction in Apoe-/- mice, and that atherosclerosis risk factors, such as cigarette smoke and hypercholesterolemia, increase mitochondrial damage in cardiovascular tissue. Follow-up studies in our lab showed that increased mitochondrial oxidative stress under hyperlipidemic conditions in aging induces atherosclerotic plaque instability in part by increasing smooth muscle cell apoptosis, necrotic core expansion, and matrix degradation. We demonstrated that targeting mitochondrial reactive oxygen species with MitoTEMPO attenuates features of atherosclerotic plaque vulnerability in middle-aged Apoe-/-/Sod2+/- mice by lowering expression of calpain-2, caspase-3, and matrix metalloproteinase-2 and decreasing smooth muscle cell apoptosis and matrix degradation.