ArticleMolecular and cellular biochemistry1999
Reduced activity of enzymes coupling ATP-generating with ATP-consuming processes in the failing myocardium.
Article in Molecular and cellular biochemistry, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 50 citations in OpenAlex.
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- Ubiquitin-proteasome-system and enzymes of energy metabolism in skeletal muscle of patients with HFpEF and HFrEF.ESC heart failure · 2021Article
- Muscular changes in animal models of heart failure with preserved ejection fraction: what comes closest to the patient?ESC heart failure · 2021Article
- Article
- Small-molecule-mediated chemical knock-down of MuRF1/MuRF2 and attenuation of diaphragm dysfunction in chronic heart failure.Journal of cachexia, sarcopenia and muscle · 2019Article
- Decline of Phosphotransfer and Substrate Supply Metabolic Circuits Hinders ATP Cycling in Aging Myocardium.PloS one · 2015Article
- Hexokinases and cardioprotection.Journal of molecular and cellular cardiology · 2015Review
- Extramitochondrial domain rich in carbonic anhydrase activity improves myocardial energetics.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Sensitivity analysis of flux determination in heart by H₂ ¹⁸O -provided labeling using a dynamic Isotopologue model of energy transfer pathways.PLoS computational biology · 2012Article
- High-energy phosphotransfer in the failing mouse heart: role of adenylate kinase and glycolytic enzymes.European journal of heart failure · 2010Article
- Methanolic extract of onion (Allium cepa) attenuates ischemia/hypoxia-induced apoptosis in cardiomyocytes via antioxidant effect.European journal of nutrition · 2009Article
- Aging-induced alterations in gene transcripts and functional activity of mitochondrial oxidative phosphorylation complexes in the heart.Mechanisms of ageing and development · 2008Article
- Heart failure: a model of cardiac and skeletal muscle energetic failure.Pflugers Archiv : European journal of physiology · 2006Review
- ATP-sensitive K+ channel channel/enzyme multimer: metabolic gating in the heart.Journal of molecular and cellular cardiology · 2005Review
- Energy metabolism in heart failure.The Journal of physiology · 2004Review
- Energetic communication between mitochondria and nucleus directed by catalyzed phosphotransfer.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Adenylate kinase phosphotransfer communicates cellular energetic signals to ATP-sensitive potassium channels.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Failing energetics in failing hearts.Current cardiology reports · 2000Review
- Phosphotransfer dynamics in skeletal muscle from creatine kinase gene-deleted mice.Molecular and cellular biochemistryArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Coupling of ATP-generating with ATP-consuming processes is an essential component in the cardiac bioenergetics responsible for optimal myocardial function. Although a number of enzymatic systems have been implicated in securing proper intracellular energy communication, their integrative response in a failing myocardium has not been determined so far. Therefore, we measured catalytic activities of enzymes responsible for the communication between ATP-generating and ATP-consuming processes in ventricular samples obtained from normal dogs and dogs with tachycardia-induced heart failure. In the failing myocardium, phosphotransfer activities of creatine kinase, adenylate kinase, 3-phosphoglycerate kinase and pyruvate kinase, which collectively deliver ATP and remove ADP from myofibrillar ATPases, were depressed by 30, 21, 44 and 20%, respectively, when compared to normal controls. The activity of hexokinase, an enzyme which directs phosphoryls into the glycolytic phosphotransfer pathway, was unchanged. Also, the activity of glyceraldehyde-3-phosphate dehydrogenase, which may shuttle inorganic phosphate between ATPases and ATP-synthases, was not affected by heart failure. However, the CO2-hydration activity of carbonic anhydrase, which together with creatine kinase, is presumed responsible for removal of protons from ATPases, was diminished by 21%. As these enzymatic systems are collectively required for adequate delivery of high-energy phosphoryl to, and removal of end-products from, cellular ATPases, the cumulative deficit in their flux capacities may provide a bioenergetic basis for impaired contraction-relaxation in the failing heart.
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Registered trials
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