GLUT1 Deficiency in Cardiomyocytes Does not Accelerate the Transition from Compensated Hypertrophy to Heart Failure

Παρόμοια τεκμήρια

• Inducible Overexpression of GLUT1 Prevents Mitochondrial Dysfunction and Attenuates Structural Remodeling in Pressure Overload but Does Not Prevent Left Ventricular Dysfunction
  ανά: Pereira, Renata O., κ.ά.
  Έκδοση: (2013)
• Maintaining PGC-1α expression following pressure overload-induced cardiac hypertrophy preserves angiogenesis but not contractile or mitochondrial function
  ανά: Pereira, Renata O., κ.ά.
  Έκδοση: (2014)
• PGC-1β Deficiency Accelerates the Transition to Heart Failure in Pressure Overload Hypertrophy: PGC-1β and Pressure Overload
  ανά: Riehle, Christian, κ.ά.
  Έκδοση: (2011)
• Loss of Bradykinin Signaling Does Not Accelerate the Development of Cardiac Dysfunction in Type 1 Diabetic Akita Mice
  ανά: Wende, Adam R., κ.ά.
  Έκδοση: (2010)
• Cardiac PI3K-Akt Impairs Insulin-Stimulated Glucose Uptake Independent of mTORC1 and GLUT4 Translocation
  ανά: Zhu, Yi, κ.ά.
  Έκδοση: (2013)