Therapeutic potential of skeletal muscle plasticity and slow muscle programming for muscular dystrophy
Duchenne muscular dystrophy (DMD) is a devastating, life-limiting, muscle disease that causes progressive, severe muscle wasting in boys and young men. There is no cure. A potential therapy may come from altering muscle phenotype based on the knowledge that slower, more oxidative muscle fibres are better protected from the dystrophic pathology than faster, more glycolytic muscle fibres. Muscle plasticity can be achieved through exercise and/or through well described pharmacological approaches such as activation of AMP-activated protein kinase (AMPK). Physical activity has many beneficial effects on muscle health but unfortunately many patients are simply unable to exercise, especially those with DMD who are usually confined to a wheelchair before their teens.
Modulating muscle activity patterns through low-frequency electrical stimulation (LFS) protocols could mimic the benefits of exercise and promote a slow muscle phenotype. No studies evaluating the therapeutic merit of LFS protocols have been conducted on the accepted mouse models of DMD nor have they determined whether muscle wasting can be attenuated or reversed. Similarly, no studies have examined the therapeutic merit of LFS in conjunction with AMPK activators. These studies are essential for enhancing the clinical translation to improve patient quality of life.
This work involves long-standing research collaboration with Professor Gregory Steinberg from Canada’s McMaster University in Hamilton, Ontario.
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