Department of Pathology, School of Medicine
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Dr. Bailey her Bachelor of Science in Zoology from the University of Oklahoma in 1989; and received her PhD in Pharmacology from the University of Oklahoma Health Science Center, College of Medicine in 1996. Her dissertation advisor: Lester A. Reinke, Dissertation title: Potential Mechanisms of Hepatic Ischemia-Reperfusion Injury. Postdoctoral Research Fellow, Department of Biochemistry, Wake Forest University School of Medicine from 3/96-2/99, Postdoctoral advisor: Carol C. Cunningham Instructor, Department of Biochemistry, Wake Forest University School of Medicine from 3/99-9/00 Assistant Professor, Department of Biochemistry, Wake Forest University School of Medicine from 10/00-8/01 Assistant Professor, Department of Environmental Health Sciences, School of Public Health, University of Alabama at Birmingham from 9/01-9/06 Associate Professor, Department of Environmental Health Sciences, School of Public Health, University of Alabama at Birmingham from 10/06 – present.
How genetic, environmental, and life-style factors influence the initiation, progression, and severity of liver diseases and how these alterations impact risk for cardiovascular disease
Our laboratory investigates the molecular mechanisms responsible for alcohol and non-alcohol (obesity) induced liver diseases. Specifically, we are interested in how mitochondrial dysfunction contributes to the pathobiology of these liver diseases through both oxidative/nitrative and bioenergetic stress. Principal areas of interests focus on understanding how disruption in nitric oxide signaling and the mitochondrial proteome contribute to the pathology of liver diseases. We are also interested in studying how genetic and environmental factors influence the initiation, progression, and severity of liver diseases.
Figure Legend. Emerging pathobiology of alcohol and obesity induced mitochondrial dysfunction and liver disease.
Strong evidence indicates that the pathogenesis of chronic alcohol and obesity/type 2 diabetes induced fatty liver disease is linked to mitochondrial dysfunction. The initial formation of an inflammatory response (increased iNOS) and increased flux of free fatty acids (FFA) enhances the production of reactive species (reactive oxygen, nitrogen, and lipid species, RONLS) in mitochondria. Similarly, associated metabolic alterations induced by these conditions leads to modifications of the mitochondrial genome and proteome. These alterations result in protein/mtDNA damage, loss in nitric oxide (NO)-mediated control of mitochondrial respiration, the inability to maintain sufficient ATP concentrations, and a further enhancement of RONLS production. Indeed, the role of oxidative/nitrative stress in these disease processes has been demonstrated in numerous experimental models.
Thus, the goal of current and future investigations will be to provide a thorough characterization of the molecular mechanisms involved in the pathogenesis of fatty liver diseases with particular emphasis on defining the role of mitochondrial stress in the disease process. A more complete understanding of the RONLS mediated effects on the spectrum of alcohol and obesity induced liver disease will facilitate the development of new mitochondrially targeted molecular medicines for treatment.