The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Mitochondrial fatty acid oxidation alterations in heart failure, ischaemic heart disease and diabetic cardiomyopathy
Open accessAbstract
Heart disease is a leading cause of death worldwide. In many forms of heart disease, including heart failure, ischaemic heart disease and diabetic cardiomyopathies, changes in cardiac mitochondrial energy metabolism contribute to contractile dysfunction and to a decrease in cardiac efficiency. Specific metabolic changes include a relative increase in cardiac fatty acid oxidation rates and an uncoupling of glycolysis from glucose oxidation. In heart failure, overall mitochondrial oxidative metabolism can be impaired while, in ischaemic heart disease, energy production is impaired due to a limitation of oxygen supply. In both of these conditions, residual mitochondrial fatty acid oxidation dominates over mitochondrial glucose oxidation. In diabetes, the ratio of cardiac fatty acid oxidation to glucose oxidation also increases, although primarily due to an increase in fatty acid oxidation and an inhibition of glucose oxidation. Recent evidence suggests that therapeutically regulating cardiac energy metabolism by reducing fatty acid oxidation and/or increasing glucose oxidation can improve cardiac function of the ischaemic heart, the failing heart and in diabetic cardiomyopathies. In this article, we review the cardiac mitochondrial energy metabolic changes that occur in these forms of heart disease, what role alterations in mitochondrial fatty acid oxidation have in contributing to cardiac dysfunction and the potential for targeting fatty acid oxidation to treat these forms of heart disease. Linked Articles: This article is part of a themed issue on Mitochondrial Pharmacology: Energy, Injury & Beyond. To view the other articles in this issue visit http://dx.doi.org/10.1111/bph.2014.171.issue‐8
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Cited by
Dunlay, S. M., Givertz, M. M., Aguilar, D., Allen, L. A., Chan, M., Desai, A. S., Deswal, A., Dickson, V. V., Kosiborod, M. N., Lekavich, C. L., et al. (2019) · Circulation · doi:10.1161/cir.0000000000000691 · Cited by 639
Lipoxidation in cardiovascular diseases
Gianazza, E., Brioschi, M., Fernandez, A. M., & Banfi, C. (2019) · Redox Biology · doi:10.1016/j.redox.2019.101119 · Cited by 152
Dunlay, S. M., Givertz, M. M., Aguilar, D., Allen, L. A., Chan, M., Desai, A. S., Deswal, A., Dickson, V. V., Kosiborod, M. N., Lekavich, C. L., et al. (2019) · Journal of Cardiac Failure · doi:10.1016/j.cardfail.2019.05.007 · Cited by 145
Mitochondrial Function and Dysfunction in Dilated Cardiomyopathy
Ramaccini, D., Montoya-Uribe, V., Aan, F. J., Modesti, L., Potes, Y., Wieckowski, M. R., Krga, I., Glibetić, M., Pinton, P., Giorgi, C., et al. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2020.624216 · Cited by 136
Roy, D., & Tedeschi, A. (2021) · Cells · doi:10.3390/cells10051078 · Cited by 68
Metadata
- Authors
- Fillmore, N., Mori, J., & Lopaschuk, G. D.
- Venue
- British Journal of Pharmacology
- Publisher
- Wiley
- Published
- 2014-03-28
- Volume
- 171
- Issue
- 8
- Pages
- 2080-2090
- ISSN
- 0007-1188 (ISSN-L)
- 1476-5381
- OpenAlex
- W1584301804
- Cited by
- 468
- References
- 7
- FWCI
- 5.65
- Type
- journal article
- Language
- en
- Open access
- bronze
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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