Skeletal muscle weakness is a hallmark of several physiological and pathological conditions, including age-associated loss of muscle mass and function (i.e. sarcopenia). Regardless of the universal impact and significance of sarcopenia in healthy lifespan, our understanding on the underlying causes of sarcopenia is still unclear. This is due to several alterations that occur with aging, including hormones, appetite, neurodegeneration, metabolism, and etc. I perform experiments to understand the mechanisms responsible for sarcopenia and eventually develop treatments that can mitigate symptoms of sarcopenia.
Oxidative stress is an imbalance between pro-oxidant and antioxidant function, which lead to cellular and tissue dysfunction in muscle. To this end, I use genetically engineered mouse models of oxidative modifications by upregulating and downregulating individual antioxidant genes in a target organ only (i.e. muscle). I study intrinsic alterations of contractile properties of skeletal muscle that are impaired with aging. This includes calcium sensitivity, calcium release and reuptake, which are critical during muscle contractile activities. I also study mitochondrial functions because mitochondria are the primary source of free radicals, calcium handling and ATP production.
My research also focuses on the role of ghrelin in sarcopenia, a hormone with decreased circulating level in the elderly. If ghrelin offers protection in animals, it would be an excellent candidate for clinical trials as it has an excellent safety profile in rodents and humans.
B.S., Physical Education, Yonsei University, South Korea, 2004
M.A., Exercise Physiology, University of North Carolina, Chapel Hill, 2011
Ph.D., Exercise Physiology, Basic and Clinical Muscle Biology Laboratory, University of Florida, 2015
Joined OMRF Scientific Staff in 2019
Ahn B, Ranjit R, Premkumar P, Pharaoh G, Piekarz KM, Matsuzaki S, Claflin DR, Riddle K, Judge J, Bhaskaran S, Satara Natarajan K, Barboza E, Wronowski B, Kinter M, Humphries KM, Griffin TM, Freeman WM, Richardson A, Brooks SV, Van Remmen H. Mitochondrial oxidative stress impairs contractile function but paradoxically increases muscle mass via fibre branching. J Cachexia Sarcopenia Muscle 10:411-428, 2019 April, PMID: 30706998, PMCID: PMC6463475
Ahn B*, Pharaoh G*, Premkumar P, Huseman K, Ranjit R, Kinter M, Szweda L, Fulop G, Tarantini S, Csiszar A, Ungvari Z, Van Remmen H. Nrf2 deficiency exacerbates age-related contractile dysfunction and loss of skeletal muscle mass. Redox Biol. 17 (2018) 47-58. PMID: 29673700 PMCID: PMC6006677 *equal contribution
Ahn B, Coblentz PD, Beharry AW, Patel N, Judge AR, Moylan JS, Hoopes CW, Bonnell MR, Ferreira LF. Diaphragm abnormalities in patients with end-stage heart failure: NADPH oxidase upregulation and protein oxidation. Front Physiol. 2017 Jan 9. PMID: 28119629 PMCID: PMC5220111
Ahn BS, Beharry AW, Frye GS, Judge AR, Ferreira LF. NAD(P)H oxidase subunit p47phox is elevated and p47phox knockout prevents diaphragm contractile dysfunction in heart failure. Am J Physiol Lung Cell Mol Physiol. 2015 Jul 24:ajplung.00176.2015. PMID: 26209274 PMCID: PMC4556931
Ahn B, Beaver T, Martin T, Hess P, Brumback BA, Ahmed S, Smith BK, Leeuwenburgh C, Martin AD, Ferreira LF. Phrenic nerve stimulation increases human diaphragm fiber force after cardiothoracic surgery. Am. J. Respir. Crit. Care Med. 2014:190:837-839.
Aging & Metabolism Research Program, MS 21
Oklahoma Medical Research Foundation
825 N.E. 13th Street
Oklahoma City, OK 73104
Phone: (405) 271-2653
Fax: (405) 271-1437