Document Detail

Inhibition of autophagy recovers cardiac dysfunction and atrophy in response to tail-suspension.
MedLine Citation:
PMID:  25476825     Owner:  NLM     Status:  Publisher    
AIMS: Physical inactivity during space flight or prolonged bed rest may cause cardiac dysfunction and atrophy, but the exact mechanism that governs the regulation of myocardial dysfunction and cardiac atrophy remains poorly understood. Autophagy, a protein degradation pathway, has recently been shown to be involved in the regulation of cardiac dysfunction and atrophy. In this study, we investigated the relationships between dysfunction and atrophy inactivity-induced and autophagy in rat cardiac tissue.
MAIN METHODS: Physical inactivity was simulated by a tail suspension model, and cardiac function was examined by echocardiography. Cardiac atrophy was measured by wheat germ agglutinin staining and autophagic activity was detected by western blot analysis and immunofluorescence staining.
KEY FINDINGS: We demonstrated that cardiac function, especially contractility, declined and the area of cardiac atrophy increased in the tail-suspended cardiac tissue. Additionally, the cross-sectional area of myocardial cells decreased; however, apoptosis did not increase with tail suspension. Similary, the expression of autophagy-related proteins and the number of autophagosomes were elevated in the tail-suspended cardiac tissue. Moreover, the administration of chloroquine, an autophagy inhibitor, reversed cardiac dysfunction and atrophy via the suppression of autophagic activity during suspension. Our results indicate that autophagy facilitates the development and progression of cardiac dysfunction and atrophy induced by tail suspension.
SIGNIFICANCE: Our studies hint that the components of the autophagy-related signaling pathway are potential therapeutic targets for the treatment of physical inactivity formed cardiac diseases.
Hong Liu; Qiong Xie; Bing-Mu Xin; Jun-Lian Liu; Yu Liu; Yong-Zhi Li; Jia-Ping Wang
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-12-1
Journal Detail:
Title:  Life sciences     Volume:  -     ISSN:  1879-0631     ISO Abbreviation:  Life Sci.     Publication Date:  2014 Dec 
Date Detail:
Created Date:  2014-12-5     Completed Date:  -     Revised Date:  2014-12-6    
Medline Journal Info:
Nlm Unique ID:  0375521     Medline TA:  Life Sci     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2014. Published by Elsevier Inc.
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