COMPENSATION FOR IMPAIRED MYOCARDIAL PHOSPHOTRANSFER IN GUANIDINOACETATE-N-METHYLTRANSFERASE KNOCKOUT MICE

Библиографические подробности
Главные авторы:	Aksentijevic, D, Lygate, C, Makinen, K, Sebag-Montefiore, L, Medway, D, Neubauer, S
Формат:	Conference item
Опубликовано:	2010

GUANIDINOACETATE N-METHYLTRANSFERASE KNOCKOUT MICE EXHIBIT NORMAL LEFT VENTRICULAR REMODELLING, HAEMODYNAMICS AND SURVIVAL AFTER MYOCARDIAL INFARCTION DESPITE LACK OF PHOSPHOCREATINE
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Adaptations to Maintain Energy Homeostasis Compensate for Creatine-Deficiency in GAMT Knockout Mice Following Myocardial Infarction, but May Contribute to Early Mitochondrial Pathology During Aging
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Guanidinoacetate N-methyltransferase-knockout mice completely lacking myocardial phosphocreatine show normal in vivo cardiac function, but increased susceptibility to ischemia/reperfusion injury
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Reduced inotropic reserve and increased susceptibility to cardiac ischemia/reperfusion injury in phosphocreatine-deficient guanidinoacetate-N-methyltransferase-knockout mice.
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Metabolic Inflexibility of Malonyl CoA Decarboxylase (MCD) Knockout Mice Leads to Cardiac Remodelling and High Mortality During Peri-Weaning Period
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Cardiac structure and function during ageing in energetically compromised Guanidinoacetate N-methyltransferase (GAMT)-knockout mice - a one year longitudinal MRI study.
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Cardiac phenotype of mitochondrial creatine kinase knockout mice is modified on a pure C57BL/6 genetic background.
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Ribose supplementation alone or with elevated creatine does not preserve high energy nucleotides or cardiac function in the failing mouse heart
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Moderate elevation of intracellular creatine by targeting the creatine transporter protects mice from acute myocardial infarction.
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Elevated Myocardial Creatine Protects Against Ischemia/Reperfusion Injury by Improving Cardiac Energetics
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Chronic creatine kinase deficiency eventually leads to congestive heart failure, but severity is dependent on genetic background, gender and age
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Chronic creatine kinase deficiency eventually leads to congestive heart failure, but severity is dependent on genetic background, gender and age.
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Cardiac dysfunction and peri-weaning mortality in malonyl-coenzyme A decarboxylase (MCD) knockout mice as a consequence of restricting substrate plasticity.
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Impaired cardiac contractile function in AGAT knockout mice devoid of creatine is rescued by homoarginine but not creatine
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Ribose Supplementation Alone or with Elevated Creatine Does Not Preserve High Energy Nucleotides or Cardiac Function in the Failing Mouse Heart.
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Regulation of myocardial creatine uptake capacity in genetically altered mouse models
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Complete absence of creatine but unaltered ATP levels in hearts from AGAT knockout mice
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Guanidinoacetate N-methyltransferase deficiency: Case report and brief review of the literature
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Phosphotransfer in Rhodobacter sphaeroides chemotaxis.
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Severely altered guanidino compound levels, disturbed body weight homeostasis and impaired fertility in a mouse model of guanidinoacetate N-methyltransferase (GAMT) deficiency.
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Mice over-expressing the myocardial creatine transporter develop progressive heart failure and show decreased glycolytic capacity.
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The creatine kinase energy transport system in the failing mouse heart
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Accelerating global left-ventricular function assessment in mice using reduced slice acquisition and three-dimensional guide-point modelling.
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COMPENSATION FOR IMPAIRED MYOCARDIAL PHOSPHOTRANSFER IN GUANIDINOACETATE-N-METHYLTRANSFERASE KNOCKOUT MICE

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