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SHR Neuro Krebs Kardio Lipid Stoffw Microb

Bugger, H; Abel, ED.
Molecular mechanisms for myocardial mitochondrial dysfunction in the metabolic syndrome.
Clin Sci (Lond). 2008; 114(3): 195-210. Doi: 10.1042/CS20070166
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Führende Autor*innen der Med Uni Graz
Bugger Heiko Matthias
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Abstract:
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.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Calcium - metabolism
Disease Models, Animal -
Fatty Acids - metabolism
Humans -
Insulin Resistance -
Metabolic Syndrome - physiopathology
Mice -
Mitochondria, Heart - physiology
Mitochondrial Myopathies - physiopathology
Oxidation-Reduction -
Oxidative Stress -
Rats -

Find related publications in this database (Keywords)
diabetes
energy metabolism
metabolic syndrome
mitochondrial dysfuction
oxidative stress
uncoupling protein (UCP)
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