Our body consists to ~50% of skeletal muscles, which are crucial for our ability to breathe and move. Skeletal muscle is also a primary site for glucose uptake and a reservoir of amino acids stored as protein. Muscle dysfunction, comprising muscle weakness and altered metabolism, is a common comorbidity in many non-communicable diseases, such as type 2 diabetes, peripheral artery disease, rheumatoid arthritis, and cancer, as well as normal ageing. Muscle dysfunction can reduce both the ability to work and the quality of life for afflicted patients and is considered to accelerate mortality.
Research projects
Our lab focuses on deciphering the molecular mechanisms that contributes to disease-induced muscle dysfunction and identifying novel therapeutic interventions to counteract muscle weakness. Altered Ca2+ handling, free radical signaling and mitochondrial function are key factors in the intramuscular interplay that may contribute to impaired muscle function and hence central components in our research.
In the lab, we currently have projects related to muscle dysfunction associated with rheumatoid arthritis (RA), obesity and type 2 diabetes (T2D) and breast cancer.
Methods
We apply a multidisciplinary translational approach involving in vivo and in vitro analysis in mice and humans, including force measurements, live imaging of Ca2+ and free radicals, metabolic profiles, mass spectrometry, and biochemical and molecular assays.
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