Silvia Carnio

TL;DR: It is demonstrated that age-related deterioration of synaptic structure and function is exacerbated by defective autophagy, which exacerbates aging phenotypes in muscle, including mitochondrial dysfunction, oxidative stress, and profound weakness.

TL;DR: Decreasing JunB expression causes muscle atrophy, whereas overexpression induces hypertrophy and blocks atrophy via myostatin inhibition and regulation of atrogin-1 and MuRF expression via FoxO3.

TL;DR: It is revealed that autophagy is critical for the preservation of mitochondrial function during damaging muscle contraction and basal oxidative stress plays a crucial role in mitochondrial maintenance during normal physical activity.

TL;DR: It is suggested that selective autophagy regulates the basal and atrophy-induced turnover of the pentameric transmembrane protein, CHRN, and that TRIM63, together with SH3GLB1 and SQSTM1 regulate this process.

TL;DR: The results indicate that nNOSμ/NO is required to regulate key homeostatic mechanisms in skeletal muscle, namely mitochondrial bioenergetics and network remodelling, UPRmt and autophagy.