熱傷と骨格筋萎縮

抄録

 After a severe burn injury, a severe and persistent systemic inflammatory syndrome develops that leads to a loss of skeletal muscle mass, otherwise referred to as muscle wasting. This is caused by the dynamic balance between skeletal muscle protein breakdown (proteolysis), skeletal muscle protein synthesis, and myogenesis being disturbed following the burn. Burns cause the activation of proteolytic processes, including the ubiquitin-proteasomal, autophagy, and apoptosis pathways; and this inhibits protein synthesis pathways, such as the insulin-like growth factor-1 pathway. Burns also inhibit skeletal muscle myogenesis by increasing the activity of negative regulators of myogenesis, such as myostatin. Furthermore, they induce neuroinflammation and motor neuron apoptosis. Because skeletal muscle atrophy induced in this way adversely affects both the survival and functional outcomes of patients, there is a need to develop novel strategies that target the molecular mechanisms involved in burn-induced skeletal muscle atrophy, such as those discussed in this review.