Living without creatine: Unchanged exercise capacity and response to chronic myocardial infarction in creatine-deficient mice

Living without creatine: Unchanged exercise capacity and response to chronic myocardial infarction in creatine-deficient mice

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RATIONALE:: Creatine is thought to be involved in the spatial and temporal buffering of ATP in energetic organs such as heart and skeletal muscle. Creatine depletion affects force generation during maximal stimulation, while reduced levels of myocardial creatine are a hallmark of the failing heart,...

Bibliográfalaš dieđut
Váldodahkkit:	Lygate, C, Aksentijevic, D, Dawson, D, Ten Hove, M, Phillips, D, De Bono, J, Medway, D, Sebag-Montefiore, L, Hunyor, I, Channon, K, Clarke, K, Zervou, S, Watkins, H, Balaban, R, Neubauer, S
Materiálatiipa:	Journal article
Giella:	English
Almmustuhtton:	2013

Geahča maid

Living without creatine: unchanged exercise capacity and response to chronic myocardial infarction in creatine-deficient mice.
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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 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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Changes in creatine transporter function during cardiac maturation in the rat.
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Complete absence of creatine but unaltered ATP levels in hearts from AGAT knockout mice
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Creatine reduces mitochondrial permeability transition pore opening in response to oxidative stress in vitro
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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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The creatine kinase energy transport system in the failing mouse heart.
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Mice over-expressing the myocardial creatine transporter develop progressive heart failure and show decreased glycolytic capacity.
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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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Unchanged mitochondrial organization and compartmentation of high-energy phosphates in creatine-deficient GAMT-/- mouse hearts.
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The creatine kinase energy transport system in the failing mouse heart
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Myocardial creatine levels do not influence response to acute oxidative stress in isolated perfused heart
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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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New insights into the creatine kinase-phosphocreatine energy buffer and transport system using mouse models of altered creatine content
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Mechanisms of creatine depletion in chronically failing rat heart.
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Hearts from gamt ko mice lack phospho-creatine, show reduced inotropic reserve and are more prone to ischemia
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Influence of homoarginine on creatine accumulation and biosynthesis in the mouse
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Almmustuhtton: (2010)

Influence of homoarginine on creatine accumulation and biosynthesis in the mouse
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Myocardial creatine uptake is regulated by the sarcolemmal fraction of the creatine transporter, but not by the total creatine transporter pool
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High-energy phosphotransfer in the failing mouse heart: role of adenylate kinase and glycolytic enzymes.
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Creatine transporter activity and content in the rat heart supplemented by and depleted of creatine.
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The creatine kinase system as a therapeutic target for myocardial ischaemia-reperfusion injury
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