Pages that link to "Q36512000"
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The following pages link to The absence of endogenous lipid oxidation in early stage heart failure exposes limits in lipid storage and turnover (Q36512000):
Displaying 50 items.
- Cardiac energy metabolic alterations in pressure overload-induced left and right heart failure (2013 Grover Conference Series) (Q26825047) (← links)
- Optimization of Cardiac Metabolism in Heart Failure (Q27023021) (← links)
- Multiphasic triacylglycerol dynamics in the intact heart during acute in vivo overexpression of CD36 (Q28573816) (← links)
- Imaging myocardial metabolic remodeling (Q30464469) (← links)
- Metabolic Remodeling in Diabetic Cardiomyopathy (Q33623469) (← links)
- SERCA1 expression enhances the metabolic efficiency of improved contractility in post-ischemic heart (Q33636306) (← links)
- Assessment of myocardial triglyceride oxidation with PET and 11C-palmitate (Q33789186) (← links)
- Substrate-enzyme competition attenuates upregulated anaplerotic flux through malic enzyme in hypertrophied rat heart and restores triacylglyceride content: attenuating upregulated anaplerosis in hypertrophy (Q34012909) (← links)
- Dietary fat supply to failing hearts determines dynamic lipid signaling for nuclear receptor activation and oxidation of stored triglyceride (Q34498562) (← links)
- Delineation of substrate selection and anaplerosis in tricarboxylic acid cycle of the heart by 13C NMR spectroscopy and mass spectrometry. (Q34911991) (← links)
- Metabolic efficiency promotes protection from pressure overload in hearts expressing slow skeletal troponin I. (Q35002176) (← links)
- Resolving confounding enrichment kinetics due to overlapping resonance signals from 13C-enriched long chain fatty acid oxidation and uptake within intact hearts (Q35185655) (← links)
- Myocardial ATGL overexpression decreases the reliance on fatty acid oxidation and protects against pressure overload-induced cardiac dysfunction (Q35739201) (← links)
- Sexual dimorphism in cardiac triacylglyceride dynamics in mice on long term caloric restriction (Q35803676) (← links)
- Enhancing Cardiac Triacylglycerol Metabolism Improves Recovery From Ischemic Stress (Q35881763) (← links)
- Ventricular assist device implantation corrects myocardial lipotoxicity, reverses insulin resistance, and normalizes cardiac metabolism in patients with advanced heart failure (Q36298248) (← links)
- Acute liver carnitine palmitoyltransferase I overexpression recapitulates reduced palmitate oxidation of cardiac hypertrophy (Q36511003) (← links)
- Novel proteins associated with human dilated cardiomyopathy: selective reduction in α(1A)-adrenergic receptors and increased desensitization proteins (Q36761037) (← links)
- The transcriptional coactivator PGC-1alpha is essential for maximal and efficient cardiac mitochondrial fatty acid oxidation and lipid homeostasis (Q36807931) (← links)
- Cardiac lipotoxicity: molecular pathways and therapeutic implications (Q36824112) (← links)
- Cardiac metabolic compensation to hypertension requires lipoprotein lipase (Q36877049) (← links)
- Acyl CoA synthetase-1 links facilitated long chain fatty acid uptake to intracellular metabolic trafficking differently in hearts of male versus female mice (Q36885497) (← links)
- Limited functional and metabolic improvements in hypertrophic and healthy rat heart overexpressing the skeletal muscle isoform of SERCA1 by adenoviral gene transfer in vivo (Q37038822) (← links)
- Energy metabolism in heart failure and remodelling (Q37090565) (← links)
- Assessing Cardiac Metabolism: A Scientific Statement From the American Heart Association. (Q37458369) (← links)
- Lipid Use and Misuse by the Heart. (Q37684850) (← links)
- Metabolic therapy at the crossroad: how to optimize myocardial substrate utilization? (Q37704721) (← links)
- Metabolic crosstalk between the heart and liver impacts familial hypertrophic cardiomyopathy. (Q37710814) (← links)
- Metabolomics as a tool for cardiac research (Q37935537) (← links)
- Myocardial triacylglycerol metabolism. (Q38025774) (← links)
- Alterations in mitochondrial function in cardiac hypertrophy and heart failure. (Q38042555) (← links)
- Cardiac metabolism and its interactions with contraction, growth, and survival of cardiomyocytes (Q38129182) (← links)
- Recent advances in metabolic imaging (Q38156683) (← links)
- Matrix revisited: mechanisms linking energy substrate metabolism to the function of the heart (Q38187952) (← links)
- Dietary management of heart failure: room for improvement? (Q38726519) (← links)
- Peroxisome proliferator-activated receptors in cardiac energy metabolism and cardiovascular disease (Q38817895) (← links)
- Peroxisome proliferator-activated receptor-α expression induces alterations in cardiac myofilaments in a pressure-overload model of hypertrophy (Q38994570) (← links)
- Metabolism in cardiomyopathy: every substrate matters (Q39232032) (← links)
- Sucrose Nonfermenting-Related Kinase Enzyme-Mediated Rho-Associated Kinase Signaling is Responsible for Cardiac Function (Q39250080) (← links)
- Metabolic remodelling in hypertrophied and failing myocardium: a review. (Q39395331) (← links)
- Effects of dietary phosphate on glucose and lipid metabolism (Q40086742) (← links)
- Common lipid features of lethal ventricular tarchyarrhythmias (LVTAs) induced by myocardial infarction and myocardial ion channel diseases (Q41042073) (← links)
- Preferential oxidation of triacylglyceride-derived fatty acids in heart is augmented by the nuclear receptor PPARalpha (Q41917508) (← links)
- Decreased rates of substrate oxidation ex vivo predict the onset of heart failure and contractile dysfunction in rats with pressure overload (Q43207763) (← links)
- Innate short-circuiting of mitochondrial metabolism in cardiac hypertrophy: identification of novel consequences of enhanced anaplerosis (Q43226935) (← links)
- Mitochondrial dysfunction caused by saturated fatty acid loading induces myocardial insulin-resistance in differentiated H9c2 myocytes: a novel ex vivo myocardial insulin-resistance model (Q43488657) (← links)
- Identification of the difference in the pathogenesis in heart failure arising from different etiologies using a microarray dataset. (Q47162144) (← links)
- Enhanced Redox State and Efficiency of Glucose Oxidation with miR Based Suppression of Maladaptive NADPH-Dependent Malic Enzyme 1 Expression in Hypertrophied Hearts. (Q49546621) (← links)
- Perilipin 5 is dispensable for normal substrate metabolism and in the adaptation of skeletal muscle to exercise training (Q51522933) (← links)
- Pathological hypertrophy and cardiac dysfunction are linked to aberrant endogenous unsaturated fatty acid metabolism. (Q55319786) (← links)