Back to Main

Faculty Detail Faculty Entry   
Name SCOTT W BALLINGER  
Campus Address BMR2 530 Zip 2180
Phone 205-934-4621
E-mail sballing@uab.edu" id="FacultyDetail1EmailAddress"><a href="mailto:sballing@uab.edu">sballing@uab.edu</a>
URL
 
 

Department Affiliations(s)
Appointment Type Department Division Rank
Center  Center for Aging  Center for Aging Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Professor
Center  Medicine  Comprehensive Diabetes Ctr Professor
Center  General Clinical Research Center  Ctr for Clinical & Translational Sci Professor
Center  Medicine  Med - Cardiovascular Disease Professor
Primary  Pathology   Joint Pathology Professor

Biographical Sketch 
Dr. Ballinger received his BS and MS degrees from Texas A&M University and his PhD degree in biochemistry from Emory University. He completed postdoctoral training at the University of Vermont's Genetics and Toxicology Laboratory, initially as an environmental pathology fellow and later as a Department of Energy Alexander Hollaender Distinguished Fellow.

Society Memberships
Organization Name Position Held Org Link
American Heart Association     
Society for Free Radical Biology and Medicine     
 

Research/Clinical Interest
Title
Environmental cardiology, free radical biology, mitochondrial function
Description
There is growing evidence that many forms of disease can be initiated by free radical mediated events or energetic deficits that can be related to cellular stress and damage. A cellular source and target of free radical production and damage is the mitochondrion. Because mitochondria are essential for multiple cell functions, including energy production, cell signaling, cell growth, proliferation, and programmed cell death, we hypothesize that free radicals cause mitochondrial damage and dysfunction in cells important in various disease processes, and furthermore, that disease risk factors increase mitochondrial damage and dysfunction. Specifically, we hypothesize that fetal and/or childhood exposure to cardiovascular disease risk factors increases the risk of adult disease development by causing mitochondrial damage and dysfunction. Finally, we also hypothesize that the mitochondrion plays a major role in influencing individual disease susceptibility by mitochondrial – nuclear interaction processes, and that environmentally influenced selection events for mitochondrial function that conveyed increased reproductive and survival success during the global establishment of human populations during prehistoric times, today, influence human disease susceptibility.

Postdoc Positions Available
Date Posted Position Title
01/14/2004  Impact of prenatal CVD risk factor exposure of adult disease development 
Studies: Impact of prenatal CVD risk factor exposure of adult disease development   
 

Selected Publications 
Publication PUBMEDID
Kryzwanski, D.M., Moellering, D., Fetterman, J.L, Dunham-Snary, K.J., Sammy, M.J., Ballinger, S.W. The Mitochondrial Genetic Paradigm for Cardiovascular Disease Susceptibility and Cellular Function: A Complementary Concept to Mendelian Genetics. Laboratory Investigation 91 (8): 1122-1135. 2011.  21647091 
Gladden JD, Ulasova E, Chen Y, Ahed M, Zellickson B, Baman M, Ballinger S.W., Darley-Usmar V, Dell’Italia LJ. Left ventricular and bioenergetic dysfunction in acute volume overload is mediated by stretch-induced cardiomyocyte xanthine oxidase activation. Free Radical Biology and Medicine. 1;51(11)1975-84 2011.
 		 21925594 
Zhai, L., Ballinger, S.W., Messina, J.L. Potential role of reactive oxygen species in injury-induced hepatic insulin resistance. Molecular Endocrinology 25 (3): 492-502, 2011.  21239612 
Harrison, C.M., Pompilius, M., Pinkerton, K.E., Ballinger, S.W. Mitochondrial oxidative stress influences atherogenic risk and cytokine induced oxidant production. Environmental Health Perspectives 119 (5): 676-681, 2011.  21169125 
Ulasova, E., Gladden, J.D., Zheng, J., Chen, Y., Pat, B., Bradley, W., Powell, P., Zhmijewski, J., Zelickson, B., Ballinger, S.W., Darley-Usmar, V., Dell’Italia, L.J. Extracellular matrix loss in acute volume overload causes structural alterations and dysfunction in cardiomyocyte subsarcolemmal mitochondria. Journal of Molecular and Cellular Cardiology 50: 147-156, 2011.  21059354 
Westbrook, D.G., Anderson, P, Pinkerton, K.E., Ballinger, S.W. Perinatal tobacco smoke exposure significantly increases vascular oxidative stress, mitochondrial damage and dysfunction in non-human primates. Cardiovascular Toxicology 10: 216 – 226 2010.   20668962 
Chuang G.C., Yang Z., Westbrook D.G., Pompilius M., Ballinger C.A., White C.R., Krzywanski D.M., Postlethwait E.M., Ballinger S.W. Pulmonary ozone exposure induces vascular dysfunction, mitochondrial damage and atherogenesis. Am J Physiol Lung Cell Mol Physiol. 297: L209-216 2009.  19395667 
Bailey, S.M., Mantena, S.K., Cakir, Y., Chhieng, D., Pinkerton, K.E., Ballinger, S.W. Ethanol and tobacco smoke increase hepatic steatosis and hypoxia in the hypercholesterolemic apoE-/-mouse: Implications for a "multi-hit" hypothesis of fatty liver disease. Free Rad. Biol. Med. 46: 928-938 (2009)  19280709 
Yang Z, Harrison CM, Chuang GC, Ballinger SW. The role of tobacco smoke induced mitochondrial damage in vascular dysfunction and atherosclerosis. Mutat Res. 2007 Aug 1;621(1-2):61-74. Epub 2007 Mar 1. Review.   17428506 
Cakir Y, Yang Z, Knight CA, Pompilius M, Westbrook D, Bailey SM, Pinkerton KE, Ballinger SW. Effect of alcohol and tobacco smoke on mtDNA damage and atherogenesis. Free Radic Biol Med. 2007 Nov 1;43(9):1279-88. Epub 2007 Jul 19.   17893041 
First Prev   1 2 of  2  Next Last  

Keywords
atherosclerosis, environmental cardiology, mitochondria, oxidative stress, evolutionary medicine

© 2003 University of Alabama School of Medicine. Copyright Information. UAB Disclaimer.
Contact the MEIS Help Desk if you experience problems with this site.