scholarly journals Some reminiscences on studies of age-dependent and activity-dependent degeneration of sensory and motor endings in mammalian skeletal muscle

2015 ◽  
Vol 227 (2) ◽  
pp. 231-236
Author(s):  
Richard R. Ribchester
Physiology ◽  
2007 ◽  
Vol 22 (4) ◽  
pp. 269-278 ◽  
Author(s):  
Stefano Schiaffino ◽  
Marco Sandri ◽  
Marta Murgia

A variety of fiber types with different contractile and metabolic properties is present in mammalian skeletal muscle. The fiber-type profile is controlled by nerve activity via specific signaling pathways, whose identification may provide potential therapeutic targets for the prevention and treatment of metabolic and neuromuscular diseases.


2010 ◽  
Vol 42 ◽  
pp. 96-97
Author(s):  
Kenneth A. Dyar ◽  
Bert Blaauw ◽  
Stefano Ciciliot ◽  
Reimar Abraham ◽  
Giorgia Pallafacchina ◽  
...  

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Joseph C. Reynolds ◽  
Rochelle W. Lai ◽  
Jonathan S. T. Woodhead ◽  
James H. Joly ◽  
Cameron J. Mitchell ◽  
...  

AbstractHealthy aging can be promoted by enhanced metabolic fitness and physical capacity. Mitochondria are chief metabolic organelles with strong implications in aging that also coordinate broad physiological functions, in part, using peptides that are encoded within their independent genome. However, mitochondrial-encoded factors that actively regulate aging are unknown. Here, we report that mitochondrial-encoded MOTS-c can significantly enhance physical performance in young (2 mo.), middle-age (12 mo.), and old (22 mo.) mice. MOTS-c can regulate (i) nuclear genes, including those related to metabolism and proteostasis, (ii) skeletal muscle metabolism, and (iii) myoblast adaptation to metabolic stress. We provide evidence that late-life (23.5 mo.) initiated intermittent MOTS-c treatment (3x/week) can increase physical capacity and healthspan in mice. In humans, exercise induces endogenous MOTS-c expression in skeletal muscle and in circulation. Our data indicate that aging is regulated by genes encoded in both of our co-evolved mitochondrial and nuclear genomes.


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