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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Review Article| January 08 2008
Molecular mechanisms for myocardial mitochondrial dysfunction in the metabolic syndrome
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 firstname.lastname@example.org).
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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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