The DOI matches its Crossref record; 93 of the 93 references it cites were found in a registry or an index.
Energy metabolism in heart failure and remodelling
Open accessAbstract
Myocytes of the failing heart undergo impressive metabolic remodelling. The time line for changes in the pathways for ATP synthesis in compensated hypertrophy is: flux through the creatine kinase (CK) reaction falls as both creatine concentration ([Cr]) and CK activity fall; increases in [ADP] and [AMP] lead to increases in glucose uptake and utilization; fatty acid oxidation either remains the same or decreases. In uncompensated hypertrophy and in other forms of heart failure, CK flux and fatty acid oxidation are both lower; any increases in glucose uptake and utilization are not sufficient to compensate for overall decreases in the capacity for ATP supply and [ATP] falls. Metabolic remodelling is under transcriptional and post-transcriptional control. The lower metabolic reserve of the failing heart contributes to impaired contractile reserve.
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Cites
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Cited by
Cardiovascular remodelling in coronary artery disease and heart failure
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Iron deficiency and heart failure: diagnostic dilemmas and therapeutic perspectives
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Rowe, G. C., Jiang, A., & Arany, Z. (2010) · Circulation Research · doi:10.1161/circresaha.110.223818 · Cited by 355
Mitochondria as a Drug Target in Ischemic Heart Disease and Cardiomyopathy
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Metadata
- Authors
- Ingwall, J. S.
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2008-10-29
- Volume
- 81
- Issue
- 3
- Pages
- 412-419
- ISSN
- 0008-6363 (ISSN-L)
- OpenAlex
- W2165274786
- Cited by
- 466
- References
- 93
- FWCI
- 16.94
- 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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