Molecular mechanisms for myocardial mitochondrial dysfunction in the metabolic syndrome.
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.
Bugger
Heiko
H
Division of Endocrinology, Metabolism and Diabetes, Program in Human Molecular Biology and Genetics, University of Utah School of Medicine, Salt Lake City, UT 84112, USA.
Abel
E Dale
ED
D000818:Animals; D002118:Calcium / Q000378:metabolism; D004195:Disease Models, Animal; D005227:Fatty Acids / Q000378:metabolism; D006801:Humans; D007333:Insulin Resistance; D024821:Metabolic Syndrome / Q000503:physiopathology*; D051379:Mice; D008929:Mitochondria, Heart / Q000502:physiology*; D017240:Mitochondrial Myopathies / Q000503:physiopathology*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D051381:Rats
D005227:Fatty Acids; D002118:Calcium