ArticleAmerican journal of physiology. Heart and circulatory physiology2013
Unchanged mitochondrial organization and compartmentation of high-energy phosphates in creatine-deficient GAMT-/- mouse hearts.
Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Maintaining energy provision in the heart: the creatine kinase system in ischaemia-reperfusion injury and chronic heart failure.Clinical science (London, England : 1979) · 2024Review
- Homoarginine and creatine deficiency do not exacerbate murine ischaemic heart failure.ESC heart failure · 2023Article
- Rat and mouse cardiomyocytes show subtle differences in creatine kinase expression and compartmentalization.PloS one · 2023Article
- Ontogeny of cardiomyocytes: ultrastructure optimization to meet the demand for tight communication in excitation-contraction coupling and energy transfer.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Review
- Mitochondrial Creatine Kinase Attenuates Pathologic Remodeling in Heart Failure.Circulation research · 2022Observational
- The Pitfalls ofFrontiers in physiology · 2021Review
- Energy-efficiency of Cardiomyocyte Stimulation with Rectangular Pulses.Scientific reports · 2019Article
- Respiration of permeabilized cardiomyocytes from mice: no sex differences, but substrate-dependent changes in the apparent ADP-affinity.Scientific reports · 2019Article
- Age-Dependent Decline in Cardiac Function in Guanidinoacetate-Frontiers in physiology · 2019Article
- IOCBIO Sparks detection and analysis software.PeerJ · 2019Article
- Impaired cardiac contractile function in arginine:glycine amidinotransferase knockout mice devoid of creatine is rescued by homoarginine but not creatine.Cardiovascular research · 2018Article
- Metabolic compartmentation in rainbow trout cardiomyocytes: coupling of hexokinase but not creatine kinase to mitochondrial respiration.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2017Article
- Decreased creatine kinase is linked to diastolic dysfunction in rats with right heart failure induced by pulmonary artery hypertension.Journal of molecular and cellular cardiology · 2015Article
- A mitochondrial basis for Huntington's disease: therapeutic prospects.Molecular and cellular biochemistry · 2014Review
- Matrix revisited: mechanisms linking energy substrate metabolism to the function of the heart.Circulation research · 2014Review
- Tight coupling of Na+/K+-ATPase with glycolysis demonstrated in permeabilized rat cardiomyocytes.PloS one · 2014Article
- The location of energetic compartments affects energetic communication in cardiomyocytes.Frontiers in physiology · 2014Article
- Role of the phosphocreatine system on energetic homeostasis in skeletal and cardiac muscles.Einstein (Sao Paulo, Brazil)Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Disruption of the creatine kinase (CK) system in hearts of CK-deficient mice leads to changes in the ultrastructure and regulation of mitochondrial respiration. We expected to see similar changes in creatine-deficient mice, which lack the enzyme guanidinoacetate methyltransferase (GAMT) to produce creatine. The aim of this study was to characterize the changes in cardiomyocyte mitochondrial organization, regulation of respiration, and intracellular compartmentation associated with GAMT deficiency. Three-dimensional mitochondrial organization was assessed by confocal microscopy. On populations of permeabilized cardiomyocytes, we recorded ADP and ATP kinetics of respiration, competition between mitochondria and pyruvate kinase for ADP produced by ATPases, ADP kinetics of endogenous pyruvate kinase, and ATP kinetics of ATPases. These data were analyzed by mathematical models to estimate intracellular compartmentation. Quantitative analysis of morphological and kinetic data as well as derived model fits showed no difference between GAMT-deficient and wild-type mice. We conclude that inactivation of the CK system by GAMT deficiency does not alter mitochondrial organization and intracellular compartmentation in relaxed cardiomyocytes. Thus, our results suggest that the healthy heart is able to preserve cardiac function at a basal level in the absence of CK-facilitated energy transfer without compromising intracellular organization and the regulation of mitochondrial energy homeostasis. This raises questions on the importance of the CK system as a spatial energy buffer in unstressed cardiomyocytes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.