Document Detail

Mitochondrial biogenesis and fragmentation as regulators of protein degradation in striated muscles.
MedLine Citation:
PMID:  22902321     Owner:  NLM     Status:  MEDLINE    
Mitochondria are dynamic organelles which adapt their morphology by fusion and fission events to the bioenergetic requirements of the cell. Cardiac and skeletal muscles are tissues with high energy demand and mitochondrial plasticity plays a key role in the homeostasis of these cells. Indeed, alterations in mitochondrial morphology, distribution and function are common features in catabolic conditions. Moreover, dysregulation of mitochondrial dynamics affects the signaling pathways that regulate muscle mass. This review discusses the recent findings of the role of mitochondrial fusion/fission and mitophagy in the control of proteolytic pathways. This article is part of a special issue entitled "Focus on Cardiac Metabolism".
Vanina Romanello; Marco Sandri
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2012-08-10
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  55     ISSN:  1095-8584     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  2013 Feb 
Date Detail:
Created Date:  2013-01-28     Completed Date:  2013-07-03     Revised Date:  2014-03-19    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  64-72     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Elsevier Ltd. All rights reserved.
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MeSH Terms
Adaptation, Biological
Carrier Proteins / genetics,  metabolism
Energy Metabolism
Mitochondria, Muscle / genetics,  metabolism*
Muscle, Skeletal / metabolism
Muscle, Striated / metabolism*
Myocardium / metabolism
Grant Support
Reg. No./Substance:
0/Carrier Proteins

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

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