ReviewJournal of Zhejiang University. Science. B2013
Metabolic remodeling in chronic heart failure.
Review in Journal of Zhejiang University. Science. B, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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.
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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.
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Who cites it
8 citing papers in PubMed.
- Pioglitazone Alleviates β1-adrenergic Receptor Antibody-induced Atrial Fibrillation SusceptivityCurrent medicinal chemistry · 2025Article
- Identification of Co-diagnostic Genes for Heart Failure and Hepatocellular Carcinoma Through WGCNA and Machine Learning Algorithms.Molecular biotechnology · 2024Article
- Chronic Heart Failure: Clinical Implications of Iron Homeostasis Disturbances Revisited.Cureus · 2022Review
- Article
- COUP-TFII revisited: Its role in metabolic gene regulation.Steroids · 2019Review
- Cardiotoxicity with vascular endothelial growth factor inhibitor therapy.NPJ precision oncology · 2018Review
- Trimetazidine attenuates pressure overload-induced early cardiac energy dysfunction via regulation of neuropeptide Y system in a rat model of abdominal aortic constriction.BMC cardiovascular disorders · 2016Article
- L-Carnitine, but not coenzyme Q10, enhances the anti-osteoporotic effect of atorvastatin in ovariectomized rats.Journal of Zhejiang University. Science. B · 2016Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the management of chronic heart failure (CHF) has made enormous progress over the past decades, CHF is still a tremendous medical and societal burden. Metabolic remodeling might play a crucial role in the pathophysiology of CHF. The characteristics and mechanisms of metabolic remodeling remained unclear, and the main hypothesis might include the changes in the availability of metabolic substrate and the decline of metabolic capability. In the early phases of the disease, metabolism shifts toward carbohydrate utilization from fatty acids (FAs) oxidation. Along with the progress of the disease, the increasing level of the hyperadrenergic state and insulin resistance cause the changes that shift back to a greater FA uptake and oxidation. In addition, a growing body of experimental and clinical evidence suggests that the improvement in the metabolic capability is likely to be more significant than the selection of the substrate.
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Registered trials
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