scholarly journals Skeletal muscle wasting with disuse atrophy is multi-dimensional: the response and interaction of myonuclei, satellite cells and signaling pathways

2014 ◽  
Vol 5 ◽  
Author(s):  
Naomi E. Brooks ◽  
Kathryn H. Myburgh
Author(s):  
Kenta Suzuki ◽  
Nayuta Hirashima ◽  
Yasuyuki Fujii ◽  
Taiki Fushimi ◽  
Ayaka Yamamoto ◽  
...  

2015 ◽  
Vol 1852 (12) ◽  
pp. 2722-2731 ◽  
Author(s):  
Daniel Moreira-Gonçalves ◽  
Ana Isabel Padrão ◽  
Rita Ferreira ◽  
Joana Justino ◽  
Rita Nogueira-Ferreira ◽  
...  

2005 ◽  
Vol 41 (1) ◽  
pp. 173 ◽  
Author(s):  
Didier Attaix ◽  
Sophie Ventadour ◽  
Audrey Codran ◽  
Daniel Béchet ◽  
Daniel Taillandier ◽  
...  

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 588
Author(s):  
Hayden W. Hyatt ◽  
Scott K. Powers

Skeletal muscle is the most abundant tissue in the body and is required for numerous vital functions, including breathing and locomotion. Notably, deterioration of skeletal muscle mass is also highly correlated to mortality in patients suffering from chronic diseases (e.g., cancer). Numerous conditions can promote skeletal muscle wasting, including several chronic diseases, cancer chemotherapy, aging, and prolonged inactivity. Although the mechanisms responsible for this loss of muscle mass is multifactorial, mitochondrial dysfunction is predicted to be a major contributor to muscle wasting in various conditions. This systematic review will highlight the biochemical pathways that have been shown to link mitochondrial dysfunction to skeletal muscle wasting. Importantly, we will discuss the experimental evidence that connects mitochondrial dysfunction to muscle wasting in specific diseases (i.e., cancer and sepsis), aging, cancer chemotherapy, and prolonged muscle inactivity (e.g., limb immobilization). Finally, in hopes of stimulating future research, we conclude with a discussion of important future directions for research in the field of muscle wasting.


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