The metabolic syndrome represents a cluster of abnormalities, including obesity, insulin resistance, dyslipidaemia and Type 2 diabetes, that increases the risk of developing cardiovascular diseases, such as coronary artery disease and heart failure. The heart failure risk is increased even after adjusting for coronary artery disease and hypertension, and evidence is emerging that changes in cardiac energy metabolism might contribute to the development of contractile dysfunction. Recent findings suggest that myocardial mitochondrial dysfunction may play an important role in the pathogenesis of cardiac contractile dysfunction in obesity, insulin resistance and Type 2 diabetes. This review will discuss potential molecular mechanisms for these mitochondrial abnormalities.
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February 2008
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Review Article|
January 08 2008
Molecular mechanisms for myocardial mitochondrial dysfunction in the metabolic syndrome
Heiko Bugger;
Heiko Bugger
1Division of Endocrinology, Metabolism and Diabetes, Program in Human Molecular Biology and Genetics, University of Utah School of Medicine, Salt Lake City, UT 84112, U.S.A.
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E. Dale Abel
1Division of Endocrinology, Metabolism and Diabetes, Program in Human Molecular Biology and Genetics, University of Utah School of Medicine, Salt Lake City, UT 84112, U.S.A.
Correspondence: Dr E. Dale Abel (email [email protected]).
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Publisher: Portland Press Ltd
Received:
May 17 2007
Revision Received:
July 23 2007
Accepted:
July 27 2007
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© The Authors Journal compilation © 2008 Biochemical Society
2008
Clin Sci (Lond) (2008) 114 (3): 195–210.
Article history
Received:
May 17 2007
Revision Received:
July 23 2007
Accepted:
July 27 2007
Citation
Heiko Bugger, E. Dale Abel; Molecular mechanisms for myocardial mitochondrial dysfunction in the metabolic syndrome. Clin Sci (Lond) 1 February 2008; 114 (3): 195–210. doi: https://doi.org/10.1042/CS20070166
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