ArticleEuropean journal of heart failure2010
High-energy phosphotransfer in the failing mouse heart: role of adenylate kinase and glycolytic enzymes.
Article in European journal of heart failure, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- Comparative analysis of metabolic and functional cardiac alterations in diet- and genetically induced mouse models of cardiac dysfunction.The FEBS journal · 2026Article
- Mechano-energetic uncoupling in heart failure.Nature reviews. Cardiology · 2025Review
- Role of AMP deaminase in diabetic cardiomyopathy.Molecular and cellular biochemistry · 2024Review
- Maintaining energy provision in the heart: the creatine kinase system in ischaemia-reperfusion injury and chronic heart failure.Clinical science (London, England : 1979) · 2024Review
- Rat and mouse cardiomyocytes show subtle differences in creatine kinase expression and compartmentalization.PloS one · 2023Article
- Subtle Role for Adenylate Kinase 1 in Maintaining Normal Basal Contractile Function and Metabolism in the Murine Heart.Frontiers in physiology · 2021Article
- Proteomic and Structural Manifestations of Cardiomyopathy in Rat Models of Obesity and Weight Loss.Frontiers in endocrinology · 2021Article
- Cardiac hypertrophy or failure? - A systematic evaluation of the transverse aortic constriction model in C57BL/6NTac and C57BL/6J substrains.Current research in physiology · 2019Article
- Immunometabolic cross-talk in the inflamed heart.Cell stress · 2019Review
- Age-Dependent Decline in Cardiac Function in Guanidinoacetate-Frontiers in physiology · 2019Article
- Actionable Metabolic Pathways in Heart Failure and Cancer-Lessons From Cancer Cell Metabolism.Frontiers in cardiovascular medicine · 2018Review
- A New Chimeric Natriuretic Peptide, CScientific reports · 2017Article
- On the pivotal role of PPARα in adaptation of the heart to hypoxia and why fat in the diet increases hypoxic injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Liver Kinase B1 complex acts as a novel modifier of myofilament function and localizes to the Z-disk in cardiac myocytes.Archives of biochemistry and biophysics · 2016Article
- LKB1/Mo25/STRAD uniquely impacts sarcomeric contractile function and posttranslational modification.Biophysical journal · 2015Article
- Cardiac dysfunction and peri-weaning mortality in malonyl-coenzyme A decarboxylase (MCD) knockout mice as a consequence of restricting substrate plasticity.Journal of molecular and cellular cardiology · 2014Article
- Cardiac metabolism in hypertrophy and heart failure: implications for therapy.Heart failure reviews · 2013Review
- Unchanged mitochondrial organization and compartmentation of high-energy phosphates in creatine-deficient GAMT-/- mouse hearts.American journal of physiology. Heart and circulatory physiology · 2013Article
- A role for thioredoxin-interacting protein (Txnip) in cellular creatine homeostasis.American journal of physiology. Endocrinology and metabolism · 2013Article
- Increases in the risk of cognitive impairment and alterations of cerebral β-amyloid metabolism in mouse model of heart failure.PloS one · 2013Article
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9 authors at 1 institution in 1 country.
Funding
Abstract
aimsTo measure the activity of the key phosphotransfer enzymes creatine kinase (CK), adenylate kinase (AK), and glycolytic enzymes in two common mouse models of chronic heart failure. METHODS AND
resultsC57BL/6 mice were subjected to transverse aortic constriction (TAC), myocardial infarction induced by coronary artery ligation (CAL), or sham operation. Activities of phosphotransfer enzymes CK, AK, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), 3-phosphoglycerate kinase (PGK), and pyruvate kinase were assessed spectrophotometrically. Mice were characterized by echocardiography or magnetic resonance imaging 5- to 8-week post-surgery and selected for the presence of congestive heart failure. All mice had severe left ventricular hypertrophy, impaired systolic function and pulmonary congestion compared with sham controls. A significant decrease in myocardial CK and maximal CK reaction velocity was observed in both experimental models of heart failure. However, the activity of AK and its isoforms remained unchanged, despite a reduction in its protein expression. In contrast, the activities of glycolytic phosphotransfer mediators GAPDH and PGK were 19 and 12% higher in TAC, and 31 and 23% higher in CAL models, respectively.
conclusionChronic heart failure in the mouse is characterized by impaired CK function, unaltered AK, and increased activity of glycolytic phosphotransfer enzymes. This pattern of altered phosphotransfer activity was observed independent of the heart failure aetiology.
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