Maintenance of an active, healthy lifestyle requires the ability to move. Skeletal muscles make up over 40% of body mass, and the proper functioning of skeletal muscle is critical for movement and maintaining an active, independent lifestyle. In my laboratory, we study how muscles respond to positive stressors, such as resistance and endurance exercise, and negative stressors, such as limb immobilization, inactivity, nerve damage, microgravity and aging. We are particularly interested in understanding why muscles lose mass and strength in response to negative stimuli, especially aging.
Muscle mass and strength peak in early adulthood and slowly decrease with advancing age. We are studying the mechanisms responsible for this process to find ways to prevent or slow the aging process. Our ultimate goal is to develop therapeutics that can prevent the loss of muscle mass and strength under various disease conditions and enhance the recovery of mass and strength following a muscle-atrophy-inducing event.
Skeletal muscle is much more than an end organ. It is one of the most plastic tissues in the body, and proper muscle function is necessary for a healthy life.
My lab studies the neuromuscular system and its response and adaptation to variety of positive and negative stressors. Skeletal muscle is a particularly interesting tissue because it interacts with and responds to numerous systems and signals to control movement, as well as glucose homeostasis, metabolism, and thermogenesis. The recent focus of my research has been on identifying the cellular and molecular mechanisms that regulate skeletal muscle mass, especially under atrophy-inducing conditions. Skeletal muscle loss occurs as the result of a variety of disparate conditions including disuse, bed rest, spinal cord injury, neurodegeneration, diabetes, cancer, chronic glucocorticoid treatment, microgravity and aging, and will affect every individual in their lifetime. Our primary goals are to identify the mechanisms responsible for muscle atrophy and determine strategies for preventing atrophy or accelerating recovery following a period of muscle loss.
Our research has identified several E3 Ubiquitin Ligases that are important regulators of skeletal muscle mass. We have utilized genetically modified mice and in vivo electroporation to examine the effect of over-expression and knock-down of selected genes on muscle mass and function. Our recent studies have focused on identification of the substrates modified by specific E3 ligases and in understanding the role of substrate ubiquitin on protein function and turnover.
In our quest to understand muscle atrophy, we have also investigated the mechanisms that regulate adaptive muscle growth in adult animals. The mechanisms regulating skeletal muscle growth are of interest since activation of anabolic pathways could be beneficial in the treatment of atrophy or in enhancing the recovery of muscle mass following an atrophy-inducing event. A current focus of the lab is identifying the mechanisms responsible for the attenuated recovery of muscle mass and function following disuse-induced atrophy in aged animals. Our ultimate goal is the development of therapeutics or therapeutic strategies that can prevent the loss of muscle mass and strength under a variety of disease conditions.
B.S., University of California, Los Angeles, 1981
M.S., University of California, Los Angeles, 1982
Ph.D., University of California, Los Angeles, 1985
Honors and Awards
Fellow of the International Union of Physiological Sciences Academy of Physiology, 2021
Honor Award, American Physiological Society Environmental and Exercise Physiology Section, 2021
Named award: “Sue C. Bodine Integrative Biology & Physiology Postdoctoral Scholar Travel Award,” UCLA Department of Integrative Biology & Physiology, 2021
Fraternal Order of Eagles Diabetes Research Chair, 2020
Edward F. Adolph Distinguished Lectureship of the American Physiological Society Environmental and Exercise Physiology Section, 2019
Fellow of the American Physiological Society, 2017
Faculty of 1000 in Pharmacology and Drug Discovery, 2014
Star Reviewer, Journal of Applied Physiology, 2010
NASA Rodent Research Science Working Group, International Space Station, 2015-present
American Physiological Society
American College of Sports Medicine
Society-Sarcopenia, Cachexia and Muscle Wasting
Gerontological Society of America
Joined OMRF scientific staff in 2023
van der Zwaard S, deLeeuw AW, Meerhoff LRA, Bodine SC, and Knobbe A. Articles with impact: insights into 10 years of research with machine learning. J. Appl. Physiol. 129: 967-979, 2020 PMID 32790596
Hughes DC, Turner DC, Baehr LM, Seaborne RA, Viggars M, Jarvis JC, Gorski PP, Stewert CE, Owens DJ, Bodine SC*, and Sharples AP*. Knockdown of the E3 ubiquitin ligase UBR5 and its role in skeletal muscle anabolism. Am J Physiol Cell Physiol. 2020 Oct 14. doi: 10.1152/ajpcell.00432.2020. Online ahead of print. PMID: 33052072
DeSousa LGO, Marshall AG, Norman JE, Fuqua JD, Lira VA, Rutledge JC, and Bodine SC. The effects of diet composition and chronic obesity on muscle growth and function. J Appl Physiol 2020 Nov 19 doi: 10.1152/japplphysiol.00156.2020 PMID 33211595
Davidyan A., Pathak S, Baar, K and Bodine SC. Maintenance of muscle mass in adult male mice is independent of testosterone. Plos one 16(3) e0240278 PMID 33764986
Baehr LM., Hughes DC., Lynch SA., Van Haver D., Maia TM., Marshall AG., Radoshevich L., Impens, F. Waddell, DS., and Bodine SC. Identification of the MuRF1 skeletal muscle ubiquitylome through quantitative proteomics. FUNCTION 10.1093/function/zqab029. PMID 34179788
Bruno NE, Nwachukwu JC, Hughes DC, Srinivasan S, Hawkins R, Sturgill D, Hager GL, Hurst S, Sheu S-S, Bodine SC, Conkright MD, Nettles KW. Activation of Crtc2/Creb1 in skeletal muscle enhances weight loss during intermittent fasting. FASEB J. 35: e21999 DOI: 10.1096/fj.202100171R. PMID 34748223