Guanidinoacetate N-methyltransferase-knockout mice completely lacking myocardial phosphocreatine show normal in vivo cardiac function, but increased susceptibility to ischemia/reperfusion injury

Gelijkaardige items

• Reduced inotropic reserve and increased susceptibility to cardiac ischemia/reperfusion injury in phosphocreatine-deficient guanidinoacetate-N-methyltransferase-knockout mice.
  door: ten Hove, M, et al.
  Gepubliceerd in: (2005)
• GUANIDINOACETATE N-METHYLTRANSFERASE KNOCKOUT MICE EXHIBIT NORMAL LEFT VENTRICULAR REMODELLING, HAEMODYNAMICS AND SURVIVAL AFTER MYOCARDIAL INFARCTION DESPITE LACK OF PHOSPHOCREATINE
  door: Lygate, C, et al.
  Gepubliceerd in: (2010)
• COMPENSATION FOR IMPAIRED MYOCARDIAL PHOSPHOTRANSFER IN GUANIDINOACETATE-N-METHYLTRANSFERASE KNOCKOUT MICE
  door: Aksentijevic, D, et al.
  Gepubliceerd in: (2010)
• Cardiac structure and function during ageing in energetically compromised Guanidinoacetate N-methyltransferase (GAMT)-knockout mice - a one year longitudinal MRI study.
  door: Schneider, J, et al.
  Gepubliceerd in: (2008)
• Supernormal myocardial creatine and phosphocreatine concentrations lead to cardiac hypertrophy and heart failure - Insights from creatine transporter over-expression transgenic mice
  door: Wallis, J, et al.
  Gepubliceerd in: (2005)