Lipid metabolism and signaling in cardiac lipotoxicity |
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| Institution: | 1. Biomedical NMR, Department of Biomedical Engineering, Eindhoven University of Technology, Den Dolech 2, 5612 AZ Eindhoven, The Netherlands;2. Department of Pediatrics, Center for Liver, Digestive and Metabolic Diseases, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713 GZ Groningen, The Netherlands;3. Department of Molecular Genetics, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands;1. Ph.D. Program for Aging, China Medical University, Taichung, Taiwan;2. Division of Cardiology, Department of Internal Medicine, China Medical University Hospital, China Medical University, Taichung, Taiwan;3. Department of Nursing, Mei Ho University, Pingguang Road, Pingtung, Taiwan;4. Department of pathology, Changhua Christian Hospital, Changhua, Taiwan;5. Jen-Teh Junior College of Medicine, Nursing and Management, Miaoli, Taiwan;6. Department of Surgery, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan;7. Chinese Medicine Department, China Medical University Beigang Hospital, Taichung, Taiwan;8. Department of Biotechnology, Bharathiar University, Coimbatore -641 046, India;9. Department of Biological Science and Technology, China Medical University, Taichung, Taiwan;10. Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan;11. Graduate Institute of Chinese Medical Science, China Medical University, Taichung, Taiwan;12. Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan |
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| Abstract: | The heart balances uptake, metabolism and oxidation of fatty acids (FAs) to maintain ATP production, membrane biosynthesis and lipid signaling. Under conditions where FA uptake outpaces FA oxidation and FA sequestration as triacylglycerols in lipid droplets, toxic FA metabolites such as ceramides, diacylglycerols, long-chain acyl-CoAs, and acylcarnitines can accumulate in cardiomyocytes and cause cardiomyopathy. Moreover, studies using mutant mice have shown that dysregulation of enzymes involved in triacylglycerol, phospholipid, and sphingolipid metabolism in the heart can lead to the excess deposition of toxic lipid species that adversely affect cardiomyocyte function. This review summarizes our current understanding of lipid uptake, metabolism and signaling pathways that have been implicated in the development of lipotoxic cardiomyopathy under conditions including obesity, diabetes, aging, and myocardial ischemia–reperfusion. This article is part of a Special Issue entitled: Heart Lipid Metabolism edited by G.D. Lopaschuk. |
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