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Cited by 499

The DOI matches its Crossref record; 91 of the 91 references it cites were found in a registry or an index.

Energy metabolism in heart failure

Ventura‐Clapier, Renée, Garnier, Anne, Veksler, Vladimir·2004·The Journal of Physiology

Abstract

Heart failure (HF) is a syndrome resulting from the inability of the cardiac pump to meet the energy requirements of the body. Despite intensive work, the pathogenesis of the cardiac intracellular abnormalities that result from HF remains incompletely understood. Factors that lead to abnormal contraction and relaxation in the failing heart include metabolic pathway abnormalities that result in decreased energy production, energy transfer and energy utilization. Heart failure also affects the periphery. Patients suffering from heart failure always complain of early muscular fatigue and exercise intolerance. This is linked in part to intrinsic alterations of skeletal muscle, among which decreases in the mitochondrial ATP production and in the transfer of energy through the phosphotransfer kinases play an important role. Alterations in energy metabolism that affect both cardiac and skeletal muscles argue for a generalized metabolic myopathy in heart failure. Recent evidence shows that decreased expression of mitochondrial transcription factors and mitochondrial proteins are involved in mechanisms causing the energy starvation in heart failure. This review will focus on energy metabolism alterations in long‐term chronic heart failure with only a few references to compensated hypertrophy when necessary. It will briefly describe the energy metabolism of normal heart and skeletal muscles and their alterations in chronic heart failure. It is beyond the scope of this review to address the metabolic switches occurring in compensated hypertrophy; readers could refer to well‐documented reviews on this subject.

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Crossref · 10.1113/jphysiol.2003.055095

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Metadata

Authors
Ventura‐Clapier, R., Garnier, A., & Veksler, V.
Venue
The Journal of Physiology
Publisher
Wiley
Published
2004-02-15
Volume
555
Issue
1
Pages
1-13
ISSN
  • 0022-3751 (ISSN-L)
  • 1469-7793
OpenAlex
W2150171020
Cited by
499
References
91
FWCI
5.47
Type
journal article
Language
en
Open access
closed

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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