Document Detail


Mouse models of mitochondrial dysfunction and heart failure.
MedLine Citation:
PMID:  15623424     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Mitochondria in the adult mammalian heart have a tremendous capacity for oxidative metabolism, and the conversion of energy by these pathways is critical for proper cardiac function. This review describes mouse models relating mitochondrial metabolism to cardiac function through gain- or loss-of-function approaches that manipulate mitochondrial energy transduction or ATP synthetic pathways. Mouse models of mitochondrial defects are relevant to genetic and acquired forms of human cardiomyopathy. Examples include inborn errors in mitochondrial metabolism or end-stage heart failure. Conversely, chronic reliance on energy production via mitochondrial fatty acid oxidation, such as occurs in the diabetic heart, likely leads to maladaptive sequelae including cellular lipotoxicity and mitochondrial dysfunction. Collectively, these model systems have allowed us to begin to dissect the relationship between mitochondrial metabolism and the development of cardiomyopathy and to define the molecular pathways regulating cardiac mitochondrial number and function.
Authors:
Laurie K Russell; Brian N Finck; Daniel P Kelly
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review     Date:  2004-12-08
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  38     ISSN:  0022-2828     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  2005 Jan 
Date Detail:
Created Date:  2004-12-29     Completed Date:  2005-05-11     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  81-91     Citation Subset:  IM    
Affiliation:
Center for Cardiovascular Research, Washington University School of Medicine, 660 South Euclid Avenue, Campus Box 8086, Saint Louis, MO 63110, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cardiomyopathies / genetics,  pathology*,  physiopathology*
Disease Models, Animal*
Fatty Acids / metabolism
Humans
Mice
Mitochondria, Heart / genetics,  metabolism*,  pathology*
Trans-Activators / metabolism
Grant Support
ID/Acronym/Agency:
K01 DK062903/DK/NIDDK NIH HHS; P01 HL5727805/HL/NHLBI NIH HHS; P30 DK52574/DK/NIDDK NIH HHS; P30 DK56341/DK/NIDDK NIH HHS; R01 DK45416/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Fatty Acids; 0/Ppargc1a protein, mouse; 0/Trans-Activators

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