JNK regulates muscle remodeling via myostatin/SMAD inhibition

Lessard, S, MacDonald, T, Pathak, P, Han, M, Coffey, V, Edge, J, Rivas, D, Hirshman, M, Davis, R and Goodyear, L 2018, 'JNK regulates muscle remodeling via myostatin/SMAD inhibition', Nature Communications, vol. 9, no. 1, pp. 1-14.


Document type: Journal Article
Collection: Journal Articles

Title JNK regulates muscle remodeling via myostatin/SMAD inhibition
Author(s) Lessard, S
MacDonald, T
Pathak, P
Han, M
Coffey, V
Edge, J
Rivas, D
Hirshman, M
Davis, R
Goodyear, L
Year 2018
Journal name Nature Communications
Volume number 9
Issue number 1
Start page 1
End page 14
Total pages 14
Publisher Nature Publishing Group
Abstract Skeletal muscle has a remarkable plasticity to adapt and remodel in response to environmental cues, such as physical exercise. Endurance exercise stimulates improvements in muscle oxidative capacity, while resistance exercise induces muscle growth. Here we show that the c-Jun N-terminal kinase (JNK) is a molecular switch that when active, stimulates muscle fibers to grow, resulting in increased muscle mass. Conversely, when muscle JNK activation is suppressed, an alternative remodeling program is initiated, resulting in smaller, more oxidative muscle fibers, and enhanced aerobic fitness. When muscle is exposed to mechanical stress, JNK initiates muscle growth via phosphorylation of the transcription factor, SMAD2, at specific linker region residues leading to inhibition of the growth suppressor, myostatin. In human skeletal muscle, this JNK/SMAD signaling axis is activated by resistance exercise, but not endurance exercise. We conclude that JNK acts as a key mediator of muscle remodeling during exercise via regulation of myostatin/SMAD signaling.
Subject Medical and Health Sciences not elsewhere classified
DOI - identifier 10.1038/s41467-018-05439-3
Copyright notice © 2018, The Author(s). Creative Commons Attribution 4.0 International License
ISSN 2041-1723
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