Eva Masiero

TL;DR: FoxO3 controls the two major systems of protein breakdown in skeletal muscle, the ubiquitin-proteasomal and autophagic/lysosomal pathways, independently and is pointed to as potential therapeutic targets in muscle wasting disorders and other degenerative and neoplastic diseases in which autophagy is involved.

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 shown that the mitochondria are removed through autophagy system and that changes in mitochondrial network occur in atrophying muscles, indicating that disruption of the mitochondrial network is an essential amplificatory loop of the muscular atrophy programme.

TL;DR: An inducible transgenic model of muscle hypertrophy by short‐term Akt activation by showing that during a fast hyper‐trophic growth myonuclear domain can increase without compromising muscle performance can be concluded.

TL;DR: Morphological, biochemical, and molecular analyses of conditional and inducible knockout mice for the critical gene Atg7, to block autophagy specifically in skeletal muscle reveal an unexpected phenotype which is characterized by muscle atrophy, weakness and features of myofiber degeneration.