Loss of muscle mass occurs in aging,a variety of diseases,including cancer,chronic heart failure,aquired immunodeficiency syndrome,diabetes,and renal failure,often aggravating pathological progression.Skeletal muscle atrophy in individuals is associated with diminished quality of life and increased health resource utilisation.Muscle wasting results from an imbalance between protein degradation and synthesis and is enhanced by decreased regenerative repair.Several signaling pathways that may contribute to muscle atrophy have been identified,and there is increasing evidence that oxidative stress,due to reactive oxygen species production plays a role in causing muscle depletion both during aging and in chronic pathological states.Hypercatabolism and in particular,oxidative stress has been proposed to enhance protein breakdown.Moreover,skeletal muscle produces a variety of secreted proteins that have important roles in intercellular communication and affects processes such as glucose homoeostasis.Preventing muscle wasting by promoting muscle growth has been proposed as a possible therapeutic approach where mainly folistatin has been widely used.In the current view,rodents where most of the experiments are performed are far away of being a good model to study the interactions at the cellular and tissue level and to discover new potential candidates in the therapies.Therefore,here,we will describe the cell model of human skeletal cells with the potential applications and impacts.