What We Do

Scientists in our program study free radicals, the highly reactive molecules capable of inducing oxidative damage to DNA, protein, and lipids. The intra- and extracellular content of these species increase during a variety of diseases. Free radical damage is therefore believed to contribute to the accompanying degeneration of physiologic function. Paradoxically, free radicals are also generated in response to normal physiologic stimuli and can exert reversible effects on protein function indicative of metabolic regulation.
The research being conducted by scientists within the Free Radical Biology and Aging Program focuses on establishing mechanisms by which free radicals regulate physiologic function and, conversely, exert deleterious effects during the progression of specific pathophysiologic events. Chemical, biochemical, and physiological approaches are employed to define pathways of free radical production and removal, structural and functional alterations to biomolecules induced by free radicals, and novel aspects of mitochondrial bioenergetics and sulfur metabolism that impact these processes.
Disease related areas of investigation focus on the role of free radicals in various pulmonary (asthma), musculoskeletal (osteoarthritis), and cardiovascular (ischemia/reperfusion and heart failure) disorders associated with the aging process and exacerbated by obesity and systemic inflammation.
Our Publications

2012
Aurora AB, Mahmoud AI, Luo X, Johnson BA, van Rooij E, Matsuzaki S, Humphries KM, Hill JA, Bassel-Duby R, Sadek HA, Olson EN. MicroRNA-214 protects the mouse heart from ischemic injury by controlling Ca2+ overload and cell death. J Clin Invest 122:1222-1232, 2012. [Abstract]
Griffin TM, Huebner JL, Kraus VB, Yan Z, Guilak F. Induction of osteoarthritis and metabolic inflammation by a very high fat diet in mice: Effects of short-term exercise. Arthritis Rheum 64:443-453, 2012. [Abstract]
Hallgren KW, Zhang D, Kinter M, Willard B, Berkner KL. Methylation of gamma-carboxylated Glu (Gla) allows detection by liquid chromatography-mass spectrometry and the identification of Gla residues in the gamma-glutamyl carboxylase. J Proteome Res 2012. [Abstract] EPub
Ziady AG, Sokolow A, Shank SL, Corey DA, Myers R, Plafker S, Kelley TJ. Interaction with CREB binding protein modulates the activities of Nrf2 AND NF-kappaB in cystic fibrosis airway epithelial cells. Am J Physiol Lung Cell Mol Physiol 2012. [Abstract] EPub
Zhu X, Castellani RJ, Moreira PI, Aliev G, Shenk JC, Siedlak SL, Harris PL, Fujioka H, Sayre LM, Szweda PA, Szweda LI, Smith MA, Perry G. Hydroxynonenal-generated crosslinking fluorophore accumulation in Alzheimer disease reveals a dichotomy of protein turnover. Free Radic Biol Med 52:699-704, 2012. [Abstract]
* Indicates publications by more than one department.
Contact Us

Free Radical Biology & Aging Research Program
Oklahoma Medical Research Foundation
825 NE 13th Street, MS 21
Oklahoma City, OK 73104
Phone: (405) 271-7570
Fax: (405) 271-1437
Email: evansj@omrf.org


