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We and others have previously demonstrated a change in metabolism during the muscle stem cell fate. This may serve to support the production of metabolites required for state-specific cell functions (such as proliferation), but may also directly regulate the muscle stem cell fate. We take an unbiased approach to profile the proteomic and metabolomic signatures of mouse muscle stem cells during different phases of skeletal muscle regeneration after a ‘physiological’ lesion induced by eccentric muscle contractions. We compare these signatures with those from muscle stem cells of dystrophic mouse muscles, which display a co-presence of stem cells at different states of their fate due to ongoing muscle injury and regeneration.

Metabolic adaptations during muscle stem cell fate are in part driven by the key energy sensor AMP-activated protein kinase (AMPK) and the kinases activated by LKB1 (i.e., the ‘AMPK-related kinases’). Our team has previously demonstrated differential cell fate adaptat