Bert Blaauw

TL;DR: The authors show that the PHD1 controls muscle mass in a hydroxylation-independent manner and prevents the degradation of leucine sensor LRS during oxygen and amino acid depletion to ensure effective mTORC1 activation in response to leucines.

TL;DR: Two major protein degradation pathways, the proteasomal and the autophagic–lysosomal pathways, are activated during muscle atrophy and variably contribute to the loss of muscle mass.

TL;DR: It is reported that muscle-specific deletion of a crucial autophagy gene, Atg7, resulted in profound muscle atrophy and age-dependent decrease in force and the results suggest that inhibition/alteration of Autophagy can contribute to myofiber degeneration and weakness in muscle disorders characterized by accumulation of abnormal mitochondria and inclusions.

TL;DR: It is reported that muscle-specific deletion of FoxO members protects from muscle loss as a result of the role of FoxOs in the induction of autophagy-lysosome and ubiquitin-proteasome systems.

TL;DR: Force activation of autophagy by genetic, dietary and pharmacological approaches restored myofiber survival and ameliorated the dystrophic phenotype of Col6a1−/− mice, indicating that defective activation of the autophagic machinery is pathogenic in some congenital muscular dystrophies.