S. Russ Price, PhD
Vice Chair & Professor
Brody 4N-84C
The Brody School of Medicine at East Carolina University
Greenville, NC 27834
phone: 252-744-2675
email: pricest17@ecu.edu
Education
- AB Zoology – University of North Carolina at Chapel Hill, 1980
- PhD Biochemistry – Brody School of Medicine, East Carolina University, 1986
- Postdoctoral Fellow – Laboratory of Cellular Metabolism, NHLBI, NIH
Research Interests
Skeletal muscle is the largest organ system in the body, composing ~50% of a healthy person’s body mass. Most people do not consider skeletal muscle to be a dynamic organ but it is. Over the course of a day, a normal adult will synthesize and degrade an amount of muscle protein equivalent to the protein content of 1.5 lb of steak. Yet, we don’t notice changes in our muscle because the processes of synthesizing and degrading proteins, collectively referred to as protein turnover, is maintained in neutral balance. In many chronic diseases such as kidney disease, diabetes or cancer, protein turnover in skeletal muscle becomes imbalanced. Protein degradation in frequently accelerated while protein synthesis is suppressed. This imbalance leads to muscle atrophy and weakness, a condition that increases a person’s risk of co-morbidities and even mortality.
I am interested in the cellular mechanisms that lead to muscle atrophy in chronic diseases, especially kidney disease and diabetes/obesity. Specific topics of interest are:
- Signaling mechanisms responsible for the increase atrophy-inducing genes that are associated with muscle loss
- Changes in microRNAs that are associated with muscle atrophy
- Functional crosstalk between skeletal muscle and other organs such as kidney and fat
- Beneficial actions of omega-3 fatty acids on muscle protein turnover
Recent Notable Publications
Pathophysiological mechanisms leading to muscle loss in chronic kidney disease. Wang XH, Mitch WE, Price SR. Nat Rev Nephrol. 2022 Mar;18(3):138-152. doi: 10.1038/s41581-021-00498-0.
MicroRNA-23a and MicroRNA-27a Mimic Exercise by Ameliorating CKD-Induced Muscle Atrophy. Wang B, Zhang C, Zhang A, Cai H, Price SR, Wang XH. J Am Soc Nephrol. 2017 Sep;28(9):2631-2640. doi: 10.1681/ASN.2016111213.
miRNA-23a/27a attenuates muscle atrophy and renal fibrosis through muscle-kidney crosstalk. Zhang A, Li M, Wang B, Klein JD, Price SR, Wang XH. J Cachexia Sarcopenia Muscle. 2018 Aug;9(4):755-770. doi: 10.1002/jcsm.12296.
Palmitate-induced ER stress and inhibition of protein synthesis in cultured myotubes does not require Toll-like receptor 4. Perry BD, Rahnert JA, Xie Y, Zheng B, Woodworth-Hobbs ME, Price SR. PLoS One. 2018 Jan 12;13(1):e0191313. doi: 10.1371/journal.pone.0191313.