Document Detail


Mitochondrial pathways in sarcopenia of aging and disuse muscle atrophy.
MedLine Citation:
PMID:  23154422     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Muscle loss during aging and disuse is a highly prevalent and disabling condition, but knowledge about cellular pathways mediating muscle atrophy is still limited. Given the postmitotic nature of skeletal myocytes, the maintenance of cellular homeostasis relies on the efficiency of cellular quality control mechanisms. In this scenario, alterations in mitochondrial function are considered a major factor underlying sarcopenia and muscle atrophy. Damaged mitochondria are not only less bioenergetically efficient, but also generate increased amounts of reactive oxygen species, interfere with cellular quality control mechanisms, and display a greater propensity to trigger apoptosis. Thus, mitochondria stand at the crossroad of signaling pathways that regulate skeletal myocyte function and viability. Studies on these pathways have sometimes provided unexpected and counterintuitive results, which suggests that they are organized into a complex, heterarchical network that is currently insufficiently understood. Untangling the complexity of such a network will likely provide clinicians with novel and highly effective therapeutics to counter the muscle loss associated with aging and disuse. In this review, we summarize the current knowledge on the mechanisms whereby mitochondrial dysfunction intervenes in the pathogenesis of sarcopenia and disuse atrophy, and highlight the prospect of targeting specific processes to treat these conditions.
Authors:
Riccardo Calvani; Anna-Maria Joseph; Peter J Adhihetty; Alfredo Miccheli; Maurizio Bossola; Christiaan Leeuwenburgh; Roberto Bernabei; Emanuele Marzetti
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Biological chemistry     Volume:  394     ISSN:  1437-4315     ISO Abbreviation:  Biol. Chem.     Publication Date:  2013 Mar 
Date Detail:
Created Date:  2013-02-05     Completed Date:  2013-08-29     Revised Date:  2014-04-10    
Medline Journal Info:
Nlm Unique ID:  9700112     Medline TA:  Biol Chem     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  393-414     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Humans
Mitochondria / pathology*
Muscular Disorders, Atrophic / physiopathology*
Oxidative Stress
Sarcopenia / physiopathology*
Signal Transduction
Grant Support
ID/Acronym/Agency:
1P30AG028740/AG/NIA NIH HHS; P30 AG028740/AG/NIA NIH HHS; R01 AG021042/AG/NIA NIH HHS; R01 DK090115/DK/NIDDK NIH HHS; R01-AG21042/AG/NIA NIH HHS; R01-DK090115-01A1/DK/NIDDK NIH HHS
Comments/Corrections

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