A novel mouse model of lipotoxic cardiomyopathy.

By Hsiu-Chiang Chiu, A. Kovács, D. Ford, F. Hsu, R. Garcia, P. Herrero, J. Saffitz, J. Schaffer. Journal of Clinical Investigation, 2001

780 citations recorded by the source corpus.

Subfields: Biochemistry, Cardiology and Cardiovascular Medicine, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/fd895dd45e89222cc6a0577eae10f35d832a901f

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Citations in the corpus

Cardiac remodeling in obesity. (2008, background): “Cardiomyocyte overexpression of acyl CoA synthase These mice develop lipotoxic cardiomyopathy, lipoapoptosis, and systolic dysfunction (51).”
Diabetic cardiomyopathy, causes and effects (2010, background): “For example, over-expression of proteins involved in cardiac FA transport such as long-chain acyl-CoA synthetase, glycosylphosphatidylinositol (GPI) membrane-anchored form of lipoprotein lipase or FA transport protein 1 resulted in lipotoxic cardiomyopathy in mice [25, 26].”
The cardiac phenotype induced by PPARalpha overexpression mimics that caused by diabetes mellitus. (2002, methodology): “(10) has shown that myocardial lipid accretion due to increased fatty acid uptake leads to myocyte apoptosis and cardiomyopathy — a “lipotoxic” effect.”
Molecular mechanisms of diabetic cardiomyopathy (2014, neutral): “Lipotoxic cardiomyopathy has been modelled in various transgenic animals in which FA uptake was increased, including overexpression of long-chain acyl-CoA synthetase 1, a glycosylphosphatidylinositol membrane-anchored form of lipoprotein lipase (LPL), or FA transport protein 1 [78–80].”
Myocardial substrate metabolism in the normal and failing heart. (2005, background): “Cardiac overexpression of FACS results in lipid accumulation, cardiac hypertrophy, gradual development of LV dysfunction, and premature death (59).”
Cardiac Metabolism and Its Interactions with Contraction, Growth, and Survival of the Cardiomyocte (2013, background): “Additional studies show that increases of lipid supply in animal models of cardiac lipotoxicity exceed the increases in the rate of oxidation, which eventually leads to downregulation of FAO, accumulation of toxic lipid intermediates, and contractile failure.(112,113) Genetic manipulations in mice t”
Intramyocardial lipid accumulation in the failing human heart resembles the lipotoxic rat heart (2004, background): “For example, cardiac-specific overexpression of acyl-CoA synthetase in mice results in marked increase in fatty acid import resulting in intramyocardial lipid overload and cardiomyopathy (22).”
Sphingolipids, insulin resistance, and metabolic disease: new insights from in vivo manipulation of sphingolipid metabolism. (2008, background): “In some cases this was shown to be associated with increases in ceramide (146, 280).”
Molecular distinction between physiological and pathological cardiac hypertrophy: experimental findings and therapeutic strategies. (2010, background): “Lipid accumulation appears to act as a trigger for cardiac myocyte hypertrophy (Chiu et al., 2001) and is evident in the failing human heart (Sharma et al.”