Cytosolic, but not mitochondrial, oxidative stress likely contributes to cardiac hypertrophy resulting from cardiac specific GLUT4 deletion in mice

Antzeko izenburuak

• Cardiac hypertrophy with preserved contractile function after selective deletion of GLUT4 from the heart
  nork: Abel, E. Dale, et al.
  Argitaratua: (1999)
• Mitochondrial adaptations to physiological vs. pathological cardiac hypertrophy
  nork: Abel, E. Dale, et al.
  Argitaratua: (2011)
• Activation of IGF-1 Receptors and Akt signaling by systemic hyperinsulinemia contributes to cardiac hypertrophy but does not regulate cardiac autophagy in obese diabetic mice
  nork: Pires, Karla Maria, et al.
  Argitaratua: (2017)
• A Conserved Role for Phosphoinositide-3-Kinase but Not Akt Signaling in Mitochondrial Adaptations that Accompany Physiological Cardiac Hypertrophy
  nork: O’Neill, Brian T., et al.
  Argitaratua: (2007)
• mTOR is a critical regulator of cardiac hypertrophy in Spontaneously Hypertensive Rats
  nork: Soesanto, Will, et al.
  Argitaratua: (2009)