ATF5 is Required for the Normal Stress Response During Skeletal Muscle Denervation

Abstract

Muscle inactivity is associated with the development of various negative health outcomes and is often accompanied by the decline in mitochondrial health. Mitochondria reside within skeletal muscle cells and are responsible for creating energy by metabolizing dietary substrates. During muscle inactivity, these mitochondria become damaged, which leads to a reduction in energy production and whole cell metabolism. To help prevent this outcome, various stress-responsive proteins within muscle cells help repair and minimize mitochondrial damage. Specifically, the stress-responsive protein ATF5 is known to help alleviate mitochondrial damage. To help understand more about these proteins in skeletal muscle, our study employed a mouse model of muscle inactivity. Our results suggest that ATF5 plays an important role in the maintenance of mitochondria and skeletal muscle health in response to muscle inactivity. This information could help us identify potential treatments for individuals experiencing severe muscle-loss related symptoms.