AI Article Synopsis

  • BDNF plays a crucial role in the differentiation and function of muscle fibers, influencing their transition from fast-twitch to slow-twitch types.
  • BDNF deletion in muscles leads to a shift from type IIB to type IIX fibers, resulting in changes that enhance resistance to fatigue but reduce motor end plate volume.
  • Conversely, overexpressing BDNF promotes fast muscle characteristics, suggesting its potential as a therapeutic target for muscle-related diseases.

Article Abstract

Brain-derived neurotrophic factor (BDNF) influences the differentiation, plasticity, and survival of central neurons and likewise, affects the development of the neuromuscular system. Besides its neuronal origin, BDNF is also a member of the myokine family. However, the role of skeletal muscle-derived BDNF in regulating neuromuscular physiology in vivo remains unclear. Using gain- and loss-of-function animal models, we show that muscle-specific ablation of BDNF shifts the proportion of muscle fibers from type IIB to IIX, concomitant with elevated slow muscle-type gene expression. Furthermore, BDNF deletion reduces motor end plate volume without affecting neuromuscular junction (NMJ) integrity. These morphological changes are associated with slow muscle function and a greater resistance to contraction-induced fatigue. Conversely, BDNF overexpression promotes a fast muscle-type gene program and elevates glycolytic fiber number. These findings indicate that BDNF is required for fiber-type specification and provide insights into its potential modulation as a therapeutic target in muscle diseases.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6690026PMC
http://dx.doi.org/10.1073/pnas.1900544116DOI Listing

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