ReviewCurrent hypertension reports2004
Energy substrate metabolism in cardiac hypertrophy.
Review in Current hypertension reports, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 66 citations in OpenAlex.
- Neuroforensomics: metabolites as valuable biomarkers in cerebrospinal fluid of lethal traumatic brain injuries.Scientific reports · 2024Article
- The dynamic interplay between cardiac mitochondrial health and myocardial structural remodeling in metabolic heart disease, aging, and heart failure.The journal of cardiovascular aging · 2023Article
- Puerarin ameliorated pressure overload-induced cardiac hypertrophy in ovariectomized rats through activation of the PPARα/PGC-1 pathway.Acta pharmacologica Sinica · 2021Article
- In vivo [U-American journal of physiology. Heart and circulatory physiology · 2020Article
- The Cardiac Lipidome in Models of Cardiovascular Disease.Metabolites · 2020Review
- Echocardiographic and Histologic Correlations in Patients with Severe Aortic Stenosis: Influence of Overweight and Obesity.Journal of cardiovascular ultrasound · 2016Article
- Normalization of cardiac substrate utilization and left ventricular hypertrophy precede functional recovery in heart failure regression.Cardiovascular research · 2016Article
- Cardiomyocyte Overexpression of FABP4 Aggravates Pressure Overload-Induced Heart Hypertrophy.PloS one · 2016Article
- Prostaglandin E Receptor Subtype 4 Signaling in the Heart: Role in Ischemia/Reperfusion Injury and Cardiac Hypertrophy.Journal of diabetes research · 2016Review
- Redox biology in pulmonary arterial hypertension (2013 Grover Conference Series).Pulmonary circulation · 2015Review
- Inhibition of hypertrophy is a good therapeutic strategy in ventricular pressure overload.Circulation · 2015Review
- Cardiac energy metabolic alterations in pressure overload-induced left and right heart failure (2013 Grover Conference Series).Pulmonary circulation · 2015Review
- Effects of hypertension and exercise on cardiac proteome remodelling.BioMed research international · 2014Review
- Cardiomyocyte autophagy: metabolic profit and loss.Heart failure reviews · 2013Review
- Propofol improves recovery of the isolated working hypertrophic heart from ischaemia-reperfusion.Pflugers Archiv : European journal of physiology · 2012Article
- Mitochondrial adaptations to physiological vs. pathological cardiac hypertrophy.Cardiovascular research · 2011Review
- Very-low-density lipoprotein: complex particles in cardiac energy metabolism.Journal of lipids · 2011Article
- Complex role of the HIF system in cardiovascular biology.Journal of molecular medicine (Berlin, Germany) · 2010Review
- Substrate uptake and metabolism are preserved in hypertrophic caveolin-3 knockout hearts.American journal of physiology. Heart and circulatory physiology · 2008Article
- Protection of the abnormal heart.Heart failure reviews · 2007Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac hypertrophy is a response to long-term pathologic (eg, hypertension) or physiologic (eg, exercise) hemodynamic overload accompanied by changes in energy substrate utilization. The pattern of substrate utilization (or metabolic phenotype) differs dramatically between pathologic and physiologic cardiac hypertrophy with directionally opposite changes in oxidation of fatty acids and glucose and glycolysis. These findings indicate that the metabolic response to long-term alterations in hemodynamic workload is not stereotypical, but is influenced by the nature of the stimulus leading to cardiac hypertrophy. Although the changes in substrate utilization are adaptive, in the case of pathologic stimuli, the changes in metabolism interfere with functional resiliency of the heart to metabolic stress, as occurs during ischemia-reperfusion. The distinct metabolic phenotypes of hearts hypertrophied in response to pathologic or physiologic stimuli are due not only to alteration in expression of metabolic enzymes and proteins, but also to post-translational modulation of metabolic enzymes and proteins.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.