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000141725 0247_ $$2doi$$a10.1093/cvr/cvy274
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000141725 0247_ $$2ISSN$$a1755-3245
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000141725 037__ $$aDKFZ-2018-01994
000141725 041__ $$aeng
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000141725 1001_ $$aMüller, Oliver J$$b0
000141725 245__ $$aComprehensive plasma and tissue profiling reveals systemic metabolic alterations in cardiac hypertrophy and failure.
000141725 260__ $$aOxford$$bOxford University Press$$c2019
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000141725 520__ $$aHeart failure is characterized by structural and metabolic cardiac remodelling. The aim of the present study is to expand our understanding of the complex metabolic alterations in the transition from pathological hypertrophy to heart failure and exploit the results from a translational perspective.Mice were subjected to transverse aortic constriction (TAC) or sham surgery and sacrificed 2, 4, or 6 weeks after the procedure. Samples from plasma, liver, skeletal muscle, and heart were collected and analysed using metabolomics. Cardiac samples were also analysed by transcriptional profiling. Progressive alterations of key cardiac metabolic pathways and gene expression patterns indicated impaired mitochondrial function and a metabolic switch during transition to heart failure. Similar to the heart, liver and skeletal muscle revealed significant metabolic alterations such as depletion of essential fatty acids and glycerolipids in late stages of heart failure. Circulating metabolites, particularly fatty acids, reflected cardiac metabolic defects and deteriorating heart function. For example, inverse correlation was found between plasma and the heart levels of triacylglycerol (C18:1, C18:2, C18:3), and sphingomyelin (d18:1, C23:0) already at an early stage of heart failure. Interestingly, combining metabolic and transcriptional data from cardiac tissue revealed that decreased carnitine shuttling and transportation preceded mitochondrial dysfunction. We, thus, studied the therapeutic potential of OCTN2 (Organic Cation/Carnitine Transporter 2), an important factor for carnitine transportation. Cardiac overexpression of OCTN2 using an adeno-associated viral (AAV) vector significantly improved ejection fraction and reduced interstitial fibrosis in mice subjected to TAC.Comprehensive plasma and tissue profiling reveals systemic metabolic alterations in heart failure, which can be used for identification of novel biomarkers and potential therapeutic targets.
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000141725 7001_ $$aHeckmann, Markus B$$b1
000141725 7001_ $$aDing, Lin$$b2
000141725 7001_ $$aRapti, Kleopatra$$b3
000141725 7001_ $$aRangrez, Ashraf Y$$b4
000141725 7001_ $$aGerken, Thomas$$b5
000141725 7001_ $$aChristiansen, Nicole$$b6
000141725 7001_ $$aRennefahrt, Ulrike E E$$b7
000141725 7001_ $$aWitt, Henning$$b8
000141725 7001_ $$aMaldonado, Sandra González$$b9
000141725 7001_ $$aTernes, Philipp$$b10
000141725 7001_ $$aSchwab, Dominic M$$b11
000141725 7001_ $$aRuf, Theresa$$b12
000141725 7001_ $$aHille, Susanne$$b13
000141725 7001_ $$aRemes, Anca$$b14
000141725 7001_ $$aJungmann, Andreas$$b15
000141725 7001_ $$aWeis, Tanja M$$b16
000141725 7001_ $$aKreußer, Julia$$b17
000141725 7001_ $$0P:(DE-He78)00a2ea610aee4a8fca32908fc3d02e91$$aGröne, Hermann-Josef$$b18$$udkfz
000141725 7001_ $$aBacks, Johannes$$b19
000141725 7001_ $$aSchatz, Philipp$$b20
000141725 7001_ $$aKatus, Hugo A$$b21
000141725 7001_ $$aFrey, Norbert$$b22
000141725 773__ $$0PERI:(DE-600)1499917-1$$a10.1093/cvr/cvy274$$n8$$p1296-1305$$tCardiovascular research$$v115$$x1755-3245$$y2019
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