Exploring new roles for the TGFβ signalling network as a cause of skeletal muscle disorders, and a target for new muscle therapeutics.
- Research Opportunity
- PhD students, Honours students, Master of Biomedical Science
- Number of Honour Places Available
- Number of Master Places Available
|A/Prof Paul Gregorevicfirstname.lastname@example.org||Personal web page|
Summary Skeletal muscle is essential for survival. Not only is muscle the vital organ for movement but the diaphragm muscle sustains life by inflating the lungs for breathing. Skeletal muscle is also an endocrine organ that contracts and releases hormones and factors that communicate with other body tissues to sustain life.
Skeletal muscle is essential for survival. Not only is muscle the vital organ for movement but the diaphragm muscle sustains life by inflating the lungs for breathing. Skeletal muscle is also an endocrine organ that contracts and releases hormones and factors that communicate with other body tissues to sustain life. Skeletal muscle accounts for half a person’s body mass yet we take for granted its crucial role in our health and lifestyle. Many diseases and conditions are linked with changes in muscle structure and function, including: ageing and frailty; cancer; muscle injury, sepsis and other forms of metabolic stress; nerve injury; disuse through inactivity and microgravity; burns; and different forms of muscular dystrophy. These conditions are major health problems globally and contribute to a large burden of disability and suffering. Tackling these muscle-related health conditions requires a coordinated research effort from discovery biology to understand disease mechanisms and translational approaches to take these discoveries from bench to the clinic. Researchers in the Centre for Muscle Research seek to understand the mechanisms that regulate muscle growth, wasting and metabolism, and to develop new approaches for preventing or treating muscle related conditions, utilising the latest techniques in biology and biomedicine. We also consider skeletal muscle in the context of other diseases, such as heart and cardiovascular diseases, cancer and osteoporosis. We are interested in understanding muscle development and growth, injury and repair, studying the biology and metabolism of muscle stem cells and their commitment to becoming functional muscle fibres. Our researchers design, manufacture and utilise viral vectors to alter gene expression in mouse models of disease and interrogate cellular mechanisms of muscle adaptation, techniques that provide a unique combination of speed, precision and efficacy not achieved through other approaches. The Centre for Muscle Research offers a wonderful training environment for studying muscle biology in health and disease and exceptional career-training opportunities for Honours, Masters and Ph.D. students.
The Transforming Growth Factor β (TGFβ) signalling network is one of the most important regulators of processes associated with skeletal muscle development, adaptation, and repair. However, many questions remain as to how this network is regulated in skeletal muscle in health and disease, how it controls processes that determine skeletal muscle characteristics, and how best to control network elements to prevent/treat muscle conditions. Combining gene delivery-based methods with cell culture and animal models and analyses of gene expression and protein regulation, this research theme seeks to examine novel processes that control the TGFβ network in skeletal muscle, and determine how unique components of the TGFβ network control skeletal muscle structure and function. These discoveries will help to develop novel strategies for preventing/treating the loss of skeletal muscle mass and strength associated with disease and advancing age.
PhD students, Honours students, Master of Biomedical Science
Students who are interested in joining this project will need to consider their elegibility as well as other requirements before contacting the supervisor of this research
For further information about this research, please contact a supervisor.
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