Loss of muscle mass and increased intramuscular fibrosis characterize both aging sarcopenia and muscular dystrophy. Research has shown that these two conditions also share some pathophysiological mechanisms including mitochondrial dysfunction, increased apoptosis, abnormal modulation of autophagy, decline in satellite cells, increased generation of reactive oxygen species, and modification of signalling and stress response pathways.
This Research Topic is intended to bring together basic researchers and clinicians working in the area of sarcopenia and muscular dystrophy in human and in animal models. The aim of this cross-fertilization is to accelerate understanding of mechanisms involved in aging and dystrophic sarcopenia and to explore the therapeutic potential of pharmacological and nutritional interventions. Contributors are encouraged to submit research articles, reviews, mini-reviews, clinical case study, perspectives, short communications as well as theoretical papers, opinions, and methods.
Loss of muscle mass and increased intramuscular fibrosis characterize both aging sarcopenia and muscular dystrophy. Research has shown that these two conditions also share some pathophysiological mechanisms including mitochondrial dysfunction, increased apoptosis, abnormal modulation of autophagy, decline in satellite cells, increased generation of reactive oxygen species, and modification of signalling and stress response pathways.
This Research Topic is intended to bring together basic researchers and clinicians working in the area of sarcopenia and muscular dystrophy in human and in animal models. The aim of this cross-fertilization is to accelerate understanding of mechanisms involved in aging and dystrophic sarcopenia and to explore the therapeutic potential of pharmacological and nutritional interventions. Contributors are encouraged to submit research articles, reviews, mini-reviews, clinical case study, perspectives, short communications as well as theoretical papers, opinions, and methods.