The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Metabolic remodelling of the failing heart: the cardiac burn-out syndrome?
Abstract
It has been postulated that the failing heart suffers from chronic energy starvation, and that derangements in cardiac energy conversion are accessory to the progressive nature of this disease. The molecular mechanisms driving this 'metabolic remodelling' process and their significance for the development of cardiac failure are still open to discussion. Next to changes in mitochondrial function, the hypertrophied heart is characterized by a marked shift in substrate preference away from fatty acids towards glucose. It has been argued that the decline in fatty acid oxidation is not fully compensated for by a rise in glucose oxidation, thereby imposing an additional burden on overall ATP generating capacity. Several lines of evidence suggest that these metabolic adaptations are brought about, at least in part, by alterations in the rate of transcription of genes encoding for proteins involved in substrate transport and metabolism. Here, the principal metabolic changes are reviewed and the various molecular mechanisms that are likely to play a role are discussed. In addition, the potential significance of these changes for the aetiology of heart failure is evaluated.
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Cites
The creatine kinase system in normal and diseased human myocardium
Ingwall, J. S., Kramer, M. F., Fifer, M. A., Lorell, B. H., Shemin, R., Grossman, W., & Allen, P. D. (1985) · New England Journal of Medicine · doi:10.1056/nejm198510243131704 · Cited by 396
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p38 Mitogen-activated Protein Kinase Activates Peroxisome Proliferator-activated Receptor α
Barger, P. M., Browning, A. C., Garner, A. N., & Kelly, D. P. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m105945200 · Cited by 260
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Construction of transgenic mice with tissue-specific acceleration of mitochondrial DNA mutagenesis
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Cited by
Lopaschuk, G. D., & Jaswal, J. S. (2010) · Journal of Cardiovascular Pharmacology · doi:10.1097/fjc.0b013e3181e74a14 · Cited by 636
Is the Failing Heart Energy Starved?: On Using Chemical Energy to Support Cardiac Function
Ingwall, J. S., & Weiss, R. G. (2004) · Circulation Research · doi:10.1161/01.res.0000137170.41939.d9 · Cited by 604
Catabolic Defect of Branched-Chain Amino Acids Promotes Heart Failure
Sun, H., Olson, K. C., Gao, C., Prosdocimo, D. A., Zhou, M., Wang, Z., Jeyaraj, D., Youn, J.-Y., Ren, S., Liu, Y., et al. (2016) · Circulation · doi:10.1161/circulationaha.115.020226 · Cited by 538
Renin-angiotensin-aldosterone system and oxidative stress in cardiovascular insulin resistance
Cooper, S. A., Whaley-Connell, A., Habibi, J., Wei, Y., Lastra, G., Manrique, C., Stas, S., & Sowers, J. R. (2007) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00522.2007 · Cited by 317
Rapamycin transiently induces mitochondrial remodeling to reprogram energy metabolism in old hearts
Chiao, Y. A., Kolwicz, S. C., Basisty, N., Gagnidze, A., Zhang, J., Gu, H., Djukovic, D., Beyer, R. P., Raftery, D., MacCoss, M., et al. (2016) · Aging · doi:10.18632/aging.100881 · Cited by 128
Metadata
- Authors
- VANBILSEN, M., SMEETS, P., GILDE, A., & VANDERVUSSE, G.
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2004-02-01
- Volume
- 61
- Issue
- 2
- Pages
- 218-226
- ISSN
- 0008-6363 (ISSN-L)
- OpenAlex
- W2104740972
- Cited by
- 261
- References
- 5
- FWCI
- 6.91
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
