Ricerc@Sapienza

Skeletal muscle mass, function, and repair capacity all progressively decline with aging, restricting mobility, voluntary function, and quality of life. Age-related reduced regenerative potential and muscle wasting, also called sarcopenia, has been in part associated with a decline in the number and function of muscle stem cells (MuSCs), the direct cellular contributors to muscle repair. Despite the clinical and social impact of sarcopenia, the age-related decline of muscle mass and function is not entirely deciphered. In our lab it has been recently demonstrated the essential role of autophagy in regulating MuSCs function and the role of STAT3 in regulating MuSCs expansion and myogenic differentiation extending its use as therapeutic target to ameliorate muscle wasting. Emerging evidences underline the importance of STAT3 signaling in modulating the autophagic process inspiring the rationale beside this project. The final outcome will be to investigate on the contribution of STAT3-mediated autophagy toward skeletal muscle repair hence counteracting muscle degeneration that occurs during aging.