Thomas Elbenhardt Jensen
Skeletal muscle is a plastic tissue that responds and adapts to external stimuli during physical activity and inactivity. Increased knowledge of the molecular signaling mechanisms that control this adaptation is not only important for understanding how the muscle reacts to work and training, but also lifestyle and aging-related diseases such as diabetes, obesity and cancer.
Inactivity and aging are associated with reduction of skeletal muscle mass and metabolic health, and exercise is effective in prevention of these adverse phenotypic changes.
Molecularly, mechanistic Target of Rapamycin Complex 1 (mTORC1) is a key regulator of muscle size, the cellular renovation process known as autophagy and metabolism, but the molecular regulation of mTORC1 remains incompletely understood, particularly in the context of muscle and exercise. The overall goal of my current research is to:
a) improve the understanding of mTORC1 regulation and function in active and inactive muscle, specifically its regulation by mechanical stress during exercise and the role of subcellular organization,
b) identify novel drug targets to modulate muscle phenotype and mTORC1 signaling.
In a major international research effort, made possible to a large part by a Novo Nordisk Foundation Excellence grant from 2015-2020, my research team will engage in a combination of powerful omics-based discovery tools (phosphoproteomics, membrane proteomics) and hypothesis-driven studies using state-of-the-art molecular cell biology and advanced microscopy techniques in muscle cells, rodent and human muscle. The results of this research are expected to have a major scientific impact on our basic knowledge of mTORC1 regulation and function in muscle and possibly drug development targeting human disease.