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CD36 Deficiency Rescues Lipotoxic Cardiomyopathy
Abstract
Obesity-related diabetes mellitus leads to increased myocardial uptake of fatty acids (FAs), resulting in a form of cardiac dysfunction referred to as lipotoxic cardiomyopathy. We have shown previously that chronic activation of the FA-activated nuclear receptor, peroxisome proliferator-activated receptor α (PPARα), is sufficient to drive the metabolic and functional abnormalities of the diabetic heart. Mice with cardiac-restricted overexpression of PPARα (myosin heavy chain [MHC]-PPARα) exhibit myocyte lipid accumulation and cardiac dysfunction. We sought to define the role of the long-chain FA transporter CD36 in the pathophysiology of lipotoxic forms of cardiomyopathy. MHC-PPARα mice were crossed with CD36-deficient mice (MHC-PPARα/CD36 −/− mice). The absence of CD36 prevented myocyte triacylglyceride accumulation and cardiac dysfunction in the MHC-PPARα mice under basal conditions and following administration of high-fat diet. Surprisingly, the rescue of the MHC-PPARα phenotype by CD36 deficiency was associated with increased glucose uptake and oxidation rather than changes in FA utilization. As predicted by the metabolic changes, the activation of PPARα target genes involved in myocardial FA-oxidation pathways in the hearts of the MHC-PPARα mice was unchanged in the CD36-deficient background. However, PPARα-mediated suppression of genes involved in glucose uptake and oxidation was reversed in the MHC-PPARα/ CD36 −/− mice. We conclude that CD36 is necessary for the development of lipotoxic cardiomyopathy in MHC-PPARα mice and that novel therapeutic strategies aimed at reducing CD36-mediated FA uptake show promise for the prevention or treatment of cardiac dysfunction related to obesity and diabetes.
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“Indeed, genetic ablation of expression of the FA transporter (CD36) reversed lipotoxicity in PPAR-α overexpressing mice (382).”
From Cardiac remodeling in obesity (2008) · cites this paper as [382]
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Metadata
- Authors
- Yang, J., Sambandam, N., Han, X., Gross, R. W., Courtois, M., Kovacs, A., Febbraio, M., Finck, B. N., & Kelly, D. P.
- Affiliations
- Cleveland Clinic (US)
- From the Center for Cardiovascular Research (J.Y., N.S., R.W.G., M.C., A.K., D.P.K.) and Departments of Medicine (J.Y., N.S., X.H., R.W.G., M.C., A.K., B.N.F., D.P.K.), Molecular Biology & Pharmacology (R.W.G., D.P.K.), and Pediatrics (D.P.K.), Washington University School of Medicine, St Louis, Mo; and Department of Cell Biology (M.F.), Lerner Research Institute, Cleveland Clinic, Ohio.
- Venue
- Circulation Research
- Published
- 2007-04-27
- Volume
- 100
- Issue
- 8
- Pages
- 1208-1217
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2160476964
- Cited by
- 246
- References
- 57
- Citations by year
- 2026: 5 · 2025: 8 · 2024: 10 · 2023: 5 · 2022: 11 · 2021: 13 · 2020: 13 · 2019: 7 · 2018: 18 · 2017: 12 · 2016: 16 · 2015: 14 · 2014: 11 · 2013: 12 · 2012: 22
- FWCI
- 7.41
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (P01HL57278, P01HL057278, P50HL077113, K08HL076452, KO8 HL076452)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30 DK-52574, P30-DK56341, P30DK056341, P30DK052574)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- CD36, lipotoxic cardiomyopathy, PPARα, fatty acid uptake, cardiac dysfunction, triglyceride accumulation, glucose uptake, glucose oxidation, fatty acid oxidation, obesity, diabetes mellitus, myosin heavy chain, high-fat diet, myocardial lipid metabolism
- MeSH terms
- Animals, Diabetic Angiopathies, Fatty Acids, Glucose, Mice, Inbred C57BL, Mice, Transgenic, Obesity, Oxidation-Reduction, Phenotype, Mice, Knockout, CD36 Antigens, PPAR alpha, Adiposity, Mice
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