Document Detail


Activation of autophagy is required for muscle homeostasis during physical exercise.
MedLine Citation:
PMID:  22082869     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Skeletal muscle fibers of collagen VI null (Col6a12/2) mice show signs of degeneration due to a block in autophagy, leading to the accumulation of damaged mitochondria and excessive apoptosis. Attempts to induce autophagic flux by subjecting these mutant mice to long-term or shorter bursts of physical activity are unsuccessful (see Grumati, et al., pp. 1415–23). In normal mice, the induction of autophagy in the skeletal muscles post-exercise is able to prevent the accumulation of damaged organelles and maintain cellular homeostasis. Thus, these studies provide an important connection between autophagy and exercise physiology.
Authors:
Usha Nair; Daniel J Klionsky
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Publication Detail:
Type:  Comment; Editorial    
Journal Detail:
Title:  Autophagy     Volume:  7     ISSN:  1554-8635     ISO Abbreviation:  Autophagy     Publication Date:  2011 Dec 
Date Detail:
Created Date:  2012-04-02     Completed Date:  2012-06-18     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  101265188     Medline TA:  Autophagy     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1405-6     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Autophagy*
Collagen Type VI / deficiency*
Muscle, Skeletal / metabolism*,  pathology*
Physical Conditioning, Animal*
Grant Support
ID/Acronym/Agency:
R01 GM053396/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Col6a1 protein, mouse; 0/Collagen Type VI
Comments/Corrections
Comment On:
Autophagy. 2011 Dec;7(12):1415-23   [PMID:  22024752 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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