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

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

Xehetasun bibliografikoak
Egile Nagusiak:	Lygate, C, Aksentijevic, D, Dawson, D, ten Hove, M, Makinen, K, Faller, K, Medway, D, Sebag-Montefiore, L, Wallis, J, Clarke, K, Watkins, H, Neubauer, S
Formatua:	Conference item
Argitaratua:	2011

Antzeko izenburuak

Hearts from gamt ko mice lack phospho-creatine, show reduced inotropic reserve and are more prone to ischemia
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Moderate elevation of intracellular creatine by targeting the creatine transporter protects mice from acute myocardial infarction.
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COMPENSATION FOR IMPAIRED MYOCARDIAL PHOSPHOTRANSFER IN GUANIDINOACETATE-N-METHYLTRANSFERASE KNOCKOUT MICE
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Regulation of Myocardial Creatine Uptake by Intra- and Extracellular Creatine Levels
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Elevated Myocardial Creatine Protects Against Ischemia/Reperfusion Injury by Improving Cardiac Energetics
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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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Creatine uptake in mouse hearts with genetically altered creatine levels.
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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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Unchanged Mitochondrial Organization and Compartmentation in Creatine Deficient GAMT-/- Mouse Heart
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Living without creatine: Unchanged exercise capacity and response to chronic myocardial infarction in creatine-deficient mice
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Living without creatine: unchanged exercise capacity and response to chronic myocardial infarction in creatine-deficient mice.
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A role for thioredoxin-interacting protein (Txnip) in cellular creatine homeostasis.
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Unchanged mitochondrial organization and compartmentation of high-energy phosphates in creatine-deficient GAMT-/- mouse hearts.
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Regulation of myocardial creatine uptake capacity in genetically altered mouse models
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REGULATION OF CELLULAR CREATINE HOMEOSTASIS: A ROLE FOR THIOREDOXIN INTERACTING PROTEIN (TXNIP)
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GUANIDINOACETATE N-METHYLTRANSFERASE KNOCKOUT MICE EXHIBIT NORMAL LEFT VENTRICULAR REMODELLING, HAEMODYNAMICS AND SURVIVAL AFTER MYOCARDIAL INFARCTION DESPITE LACK OF PHOSPHOCREATINE
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Supernormal myocardial creatine and phosphocreatine concentrations lead to cardiac hypertrophy and heart failure - Insights from creatine transporter over-expression transgenic mice
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Supra-normal (phospho-)creatine levels lead to heart failure in mice overexpressing the cardiac creatine transporter - a longitudinal study
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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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Complete absence of creatine but unaltered ATP levels in hearts from AGAT knockout mice
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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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High energy phosphotransfer in the failing mouse heart-role of adenylate kinase and glycolytic enzymes
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Supranormal myocardial creatine and phosphocreatine concentrations lead to cardiac hypertrophy and heart failure: insights from creatine transporter-overexpressing transgenic mice.
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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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Changes in creatine transporter function during cardiac maturation in the rat.
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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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Metabolic Inflexibility of Malonyl CoA Decarboxylase (MCD) Knockout Mice Leads to Cardiac Remodelling and High Mortality During Peri-Weaning Period
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The creatine kinase energy transport system in the failing mouse heart
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High-energy phosphotransfer in the failing mouse heart: role of adenylate kinase and glycolytic enzymes.
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New insights into the creatine kinase-phosphocreatine energy buffer and transport system using mouse models of altered creatine content
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Chronic Creatine-deficiency is not the Underlying Cause of Cardiac Dysfunction in Mice Lacking the Creatine Biosynthetic Enzyme Arginine: glycine Amidinotransferase
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Mice over-expressing the myocardial creatine transporter develop progressive heart failure and show decreased glycolytic capacity.
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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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Reduced inotropic reserve and increased susceptibility to cardiac ischemia/reperfusion injury in phosphocreatine-deficient guanidinoacetate-N-methyltransferase-knockout mice.
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Myocardial creatine levels do not influence response to acute oxidative stress in isolated perfused heart
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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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Creatine reduces mitochondrial permeability transition pore opening in response to oxidative stress in vitro
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Mechanisms of creatine depletion in chronically failing rat heart.
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