Myocardial fatty acid metabolism in health and disease.
- G. Lopaschuk, J. Ussher, Clifford D. L. Folmes, J. Jaswal, W. Stanley
- MedicinePhysiological Reviews
The regulation of myocardial fatty acid beta-oxidation is reviewed and how alterations in fatty acid Beta-Oxidation can contribute to heart disease is discussed.
Myocardial substrate metabolism in the normal and failing heart.
- W. Stanley, F. Recchia, G. Lopaschuk
- Biology, MedicinePhysiological Reviews
- 1 July 2005
This review discusses the metabolic changes that occur in chronic heart failure, with emphasis on the mechanisms that regulate the changes in the expression of metabolic genes and the function of metabolic pathways and the consequences of these metabolic changes on cardiac function.
A mitochondria-K+ channel axis is suppressed in cancer and its normalization promotes apoptosis and inhibits cancer growth.
- S. Bonnet, S. Archer, E. Michelakis
- BiologyCancer Cell
Mitochondrial overload and incomplete fatty acid oxidation contribute to skeletal muscle insulin resistance.
The cardiac phenotype induced by PPARalpha overexpression mimics that caused by diabetes mellitus.
- B. Finck, J. J. Lehman, D. Kelly
- Biology, MedicineJournal of Clinical Investigation
PPARalpha is a critical regulator of myocardial fatty acid uptake and utilization, activation of cardiac PPARalpha regulatory pathways results in a reciprocal repression of glucose uptake and usage pathways, and derangements in myocardian energy metabolism typical of the diabetic heart can become maladaptive, leading to cardiomyopathy.
Regulation of myocardial carbohydrate metabolism under normal and ischaemic conditions. Potential for pharmacological interventions.
- W. Stanley, G. Lopaschuk, J. Hall, J. G. Mccormack
- Medicine, BiologyCardiovascular Research
- 1 February 1997
Regulation of fatty acid oxidation in the mammalian heart in health and disease.
- G. Lopaschuk, D. Belke, J. Gamble, T. Itoi, B. Schönekess
- BiologyBiochimica et Biophysica Acta
- 4 August 1994
The antianginal drug trimetazidine shifts cardiac energy metabolism from fatty acid oxidation to glucose oxidation by inhibiting mitochondrial long-chain 3-ketoacyl coenzyme A thiolase.
- P. Kantor, A. Lucien, R. Kozak, G. Lopaschuk
- Biology, ChemistryCirculation Research
- 17 March 2000
The data suggest that the antianginal effects of trimetazidine may occur because of an inhibition of long-chain 3-ketoacyl CoA thiolase activity, which results in a reduction in fatty acid oxidation and a stimulation of glucose oxidation.
Pathways and control of ketone body metabolism: on the fringe of lipid biochemistry.
- T. Fukao, G. Lopaschuk, G. Mitchell
- BiologyProstaglandins, Leukotrienes and Essential Fatty…
- 1 March 2004
AMPK alterations in cardiac physiology and pathology: enemy or ally?
- J. Dyck, G. Lopaschuk
- Biology, MedicineJournal of Physiology
- 1 July 2006
The issue of whether AMPK activation acts as an enemy or ally to the ischaemic and hypertrophied heart is addressed and has important implications as to whether therapeutic approaches to protect theIschaemic heart should be developed which either activate or inhibit AMPK.