The failing heart--an engine out of fuel.
By S. Neubauer. New England Journal of Medicine, 2007
2,352 citations recorded by the source corpus.
Subfields: Cardiology and Cardiovascular Medicine
View Paper: https://www.semanticscholar.org/paper/1466ce9c4d6443c7689d8223792f56c3ec2749d3
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In Cardiology and Cardiovascular Medicine
Citations in the corpus
- Cardiac Energy Metabolism in Heart Failure (2021, methodology): “This can be achieved by increasing circulating ketone body levels, primarily by one of the 4 following approaches: (1) ketone infusions, (2) ketone ester administration, (3) SGLT2 (sodium/glucose co-transporter 2) inhibitors, and (4) administration of a ketogenic diet.”
- Cardiac Metabolism in Heart Failure - Implications beyond ATP production (2013, neutral): “Given that sufficient ATP supply is essential for normal cardiac function, this change has been suggested to be responsible for the transition to systolic dysfunction.(6,84) If this were true, it would be reasonable to hypothesize that ATP depletion should be detectable in compensated Figure 2.”
- Molecular distinction between physiological and pathological cardiac hypertrophy: experimental findings and therapeutic strategies. (2010, background): “Of note, in advanced pathological hypertrophy and failure, glucose metabolism decreases as the heart becomes resistant to insulin, reducing the overall ability of the heart to generate sufficient ATP (see Neubauer, 2007).”
- The Failing Heart Relies on Ketone Bodies as a Fuel (2016, background): “Notably, the [phosphocreatine]/[ATP] ratio correlates with heart failure severity and is a strong predictor of cardiovascular mortality.(11,12) In addition, studies conducted in animal models have consistently revealed reprogramming of myocardial fuel utilization in the hypertrophied and failing hea”
- Narrative Review (2012, background): “Chronic HF is characterized by sympathetic activation, b-receptor downregulation, and a failure of cardiac energy metabolism.(83) When the failing heart is stimulated with b-agonists or phosphodiesterase inhibitors free ADP concentrations increase to a value that is approximately twice that of the n”
- Multi-dimensional roles of ketone bodies in fuel metabolism, signaling, and therapeutics (2017, background): “Genetically programmed abnormalities of cardiac fuel metabolism in mouse models provoke cardiomyopathy (Carley et al., 2014; Neubauer, 2007).”
- Transcriptional control of mitochondrial biogenesis: the central role of PGC-1alpha. (2008, background): “The energetic failure of the hypertrophied and failing heart has been extensively reviewed elsewhere (for example see reference 72–76 ).”
- Mechanisms of Cardiovascular Benefits of Sodium Glucose Co-Transporter 2 (SGLT2) Inhibitors (2020, background): “Mitochondrial glucose oxidation decreases in the failing heart (26–28), leading to a decrease in energy production and a fuelstarved heart (29).”
- Regulation of pyruvate metabolism and human disease (2013, background): “This disorder affects approximately 2 % of the US population and increases to 6–10 % of people over age 65, representing an incredible burden on the US healthcare system [240, 241].”
- Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets (2015, background): “Free creatine which is created from the removal of phosphate from PCr diffuses back into the mitochondria (Neubauer 2007).”
- Cardiac Metabolism and Its Interactions with Contraction, Growth, and Survival of the Cardiomyocte (2013, result): “This is reflected as a decreased PCr/ATP ratio and eventually, as compensated hypertrophy advances to overt heart failure, significant decreases of ATP are observed.(84,85) The PCr/ATP ratio has been shown to be a superior predictor of mortality as compared with ejection fraction (EF) in patients wi”