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

Show other versions (1)

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,...

ver descrição completa

Detalhes bibliográficos
Main Authors:	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
Formato:	Journal article
Idioma:	English
Publicado em:	2013

Registos relacionados

Living without creatine: unchanged exercise capacity and response to chronic myocardial infarction in creatine-deficient mice.
Por: Lygate, C, et al.
Publicado em: (2013)

Moderate elevation of intracellular creatine by targeting the creatine transporter protects mice from acute myocardial infarction.
Por: Lygate, C, et al.
Publicado em: (2012)

Regulation of Myocardial Creatine Uptake by Intra- and Extracellular Creatine Levels
Por: Makinen, K, et al.
Publicado em: (2008)

Elevated Myocardial Creatine Protects Against Ischemia/Reperfusion Injury by Improving Cardiac Energetics
Por: Lygate, C, et al.
Publicado em: (2011)

Creatine uptake in mouse hearts with genetically altered creatine levels.
Por: ten Hove, M, et al.
Publicado em: (2008)

Chronic creatine kinase deficiency eventually leads to congestive heart failure, but severity is dependent on genetic background, gender and age
Por: Lygate, C, et al.
Publicado em: (2012)

Chronic creatine kinase deficiency eventually leads to congestive heart failure, but severity is dependent on genetic background, gender and age.
Por: Lygate, C, et al.
Publicado em: (2012)

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
Por: Lygate, C, et al.
Publicado em: (2011)

Cardiac phenotype of mitochondrial creatine kinase knockout mice is modified on a pure C57BL/6 genetic background.
Por: Lygate, C, et al.
Publicado em: (2009)

Supra-normal (phospho-)creatine levels lead to heart failure in mice overexpressing the cardiac creatine transporter - a longitudinal study
Por: ten Hove, M, et al.
Publicado em: (2006)

A role for thioredoxin-interacting protein (Txnip) in cellular creatine homeostasis.
Por: Zervou, S, et al.
Publicado em: (2013)

Ribose supplementation alone or with elevated creatine does not preserve high energy nucleotides or cardiac function in the failing mouse heart
Por: Faller, K, et al.
Publicado em: (2013)

REGULATION OF CELLULAR CREATINE HOMEOSTASIS: A ROLE FOR THIOREDOXIN INTERACTING PROTEIN (TXNIP)
Por: Zervou, S, et al.
Publicado em: (2013)

Changes in creatine transporter function during cardiac maturation in the rat.
Por: Fischer, A, et al.
Publicado em: (2010)

Complete absence of creatine but unaltered ATP levels in hearts from AGAT knockout mice
Por: ten Hove, M, et al.
Publicado em: (2007)

Supernormal myocardial creatine and phosphocreatine concentrations lead to cardiac hypertrophy and heart failure - Insights from creatine transporter over-expression transgenic mice
Por: Wallis, J, et al.
Publicado em: (2005)

Unchanged Mitochondrial Organization and Compartmentation in Creatine Deficient GAMT-/- Mouse Heart
Por: Branovets, J, et al.
Publicado em: (2013)

Regulation of myocardial creatine uptake capacity in genetically altered mouse models
Por: Ten Hove, M, et al.
Publicado em: (2007)

Supranormal myocardial creatine and phosphocreatine concentrations lead to cardiac hypertrophy and heart failure: insights from creatine transporter-overexpressing transgenic mice.
Por: Wallis, J, et al.
Publicado em: (2005)

Creatine reduces mitochondrial permeability transition pore opening in response to oxidative stress in vitro
Por: Zervou, S, et al.
Publicado em: (2010)

Chronic Creatine-deficiency is not the Underlying Cause of Cardiac Dysfunction in Mice Lacking the Creatine Biosynthetic Enzyme Arginine: glycine Amidinotransferase
Por: Lygate, C, et al.
Publicado em: (2013)

The creatine kinase energy transport system in the failing mouse heart.
Por: Lygate, C, et al.
Publicado em: (2007)

Mice over-expressing the myocardial creatine transporter develop progressive heart failure and show decreased glycolytic capacity.
Por: Phillips, D, et al.
Publicado em: (2010)

Impaired cardiac contractile function in AGAT knockout mice devoid of creatine is rescued by homoarginine but not creatine
Por: Faller, K, et al.
Publicado em: (2017)

Unchanged mitochondrial organization and compartmentation of high-energy phosphates in creatine-deficient GAMT-/- mouse hearts.
Por: Branovets, J, et al.
Publicado em: (2013)

The creatine kinase energy transport system in the failing mouse heart
Por: Lygate, C, et al.
Publicado em: (2006)

Myocardial creatine levels do not influence response to acute oxidative stress in isolated perfused heart
Por: Aksentijević, D, et al.
Publicado em: (2014)

Ribose Supplementation Alone or with Elevated Creatine Does Not Preserve High Energy Nucleotides or Cardiac Function in the Failing Mouse Heart.
Por: Kiterie M E Faller, et al.
Publicado em: (2013-01-01)

New insights into the creatine kinase-phosphocreatine energy buffer and transport system using mouse models of altered creatine content
Por: Lygate, C, et al.
Publicado em: (2006)

Mechanisms of creatine depletion in chronically failing rat heart.
Por: Ten Hove, M, et al.
Publicado em: (2005)

Hearts from gamt ko mice lack phospho-creatine, show reduced inotropic reserve and are more prone to ischemia
Por: ten Hove, M, et al.
Publicado em: (2005)

Influence of homoarginine on creatine accumulation and biosynthesis in the mouse
Por: Lygate, CA, et al.
Publicado em: (2022)

GUANIDINOACETATE N-METHYLTRANSFERASE KNOCKOUT MICE EXHIBIT NORMAL LEFT VENTRICULAR REMODELLING, HAEMODYNAMICS AND SURVIVAL AFTER MYOCARDIAL INFARCTION DESPITE LACK OF PHOSPHOCREATINE
Por: Lygate, C, et al.
Publicado em: (2010)

Influence of homoarginine on creatine accumulation and biosynthesis in the mouse
Por: Craig A. Lygate, et al.
Publicado em: (2022-08-01)

Metabolic Inflexibility of Malonyl CoA Decarboxylase (MCD) Knockout Mice Leads to Cardiac Remodelling and High Mortality During Peri-Weaning Period
Por: Aksentijevic, D, et al.
Publicado em: (2014)

Myocardial creatine uptake is regulated by the sarcolemmal fraction of the creatine transporter, but not by the total creatine transporter pool
Por: Boehm, E, et al.
Publicado em: (2002)

COMPENSATION FOR IMPAIRED MYOCARDIAL PHOSPHOTRANSFER IN GUANIDINOACETATE-N-METHYLTRANSFERASE KNOCKOUT MICE
Por: Aksentijevic, D, et al.
Publicado em: (2010)

High-energy phosphotransfer in the failing mouse heart: role of adenylate kinase and glycolytic enzymes.
Por: Aksentijević, D, et al.
Publicado em: (2010)

Creatine transporter activity and content in the rat heart supplemented by and depleted of creatine.
Por: Boehm, E, et al.
Publicado em: (2003)

The creatine kinase system as a therapeutic target for myocardial ischaemia-reperfusion injury
Por: Cao, F, et al.
Publicado em: (2018)