Vanina Romanello

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: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.

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: 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: It is found that sedentary but not active humans display an age-related decline in the mitochondrial protein, optic atrophy 1 (OPA1), that is associated with muscle loss and can trigger a cascade of signaling initiated at the ER that systemically affects general metabolism and aging.