myosin heavy chain

muscular dystrophy

muscle function

satellite cells

muscle fibers

energy metabolism

Proceedings of the National Academy of Sciences

Significance The brain-derived neurotrophic factor (BDNF) is essential to promote neuronal differentiation, plasticity, and survival. Altered BDNF expression is associated with several pathologies, including neuropsychiatric and neurodegenerative disorders, cardiovascular diseases, diabetes, and motor neuron diseases. Although BDNF has been identified as a contraction-induced myokine, its involvement in muscle physiology is unclear. Using functional, cellular, and molecular approaches, we report here that the myokine BDNF regulates glycolytic muscle fiber-type identity. Our findings warrant additional studies to determine whether modulating the activity of BDNF represents an effective therapeutic strategy to delay or even prevent muscle wasting disorders in which the function of glycolytic muscle fibers is compromised (e.g., in Duchenne muscular dystrophy, muscle insulin resistance).

BDNF is a mediator of glycolytic fiber-type specification in mouse skeletal muscle