P38α MAPK coordinates the activities of several metabolic pathways that together induce atrophy of denervated muscles.

Physiological or pathological muscle disuse/inactivity or loss of the neural-muscular junction cause muscle atrophy. Atrophy-inducing conditions cause metabolic oxidative stress in the muscle tissue, activation of the ubiquitin-proteasome and of the autophagosome-lysosome systems, enhanced removal of the damaged proteins and organelles, and loss of muscle mass and strength. The signaling pathways that control these catabolic processes are only partially known.

Adhesion molecule Kirrel3/Neph2 is required for the elongated shape of myocytes during skeletal muscle differentiation.

Kirrel/Neph proteins are evolutionarily conserved members of the immunoglobulin superfamily of adhesion proteins. Kirrel3 is the mouse orthologue of Dumbfounded (Duf), a family member that regulates myoblast pre-fusion events in Drosophila. Yet, the role of Kirrel3 in mammalian myogenesis has not been demonstrated.