Glycogen Synthase Kinase-3α Reduces Cardiac Growth and Pressure Overload-induced Cardiac Hypertrophy by Inhibition of Extracellular Signal-regulated Kinases
Peiyong Zhai(Rutgers, The State University of New Jersey), Junichi Sadoshima(Rutgers, The State University of New Jersey)
Cited by 68
Related Papers
Nicotinamide Mononucleotide, an Intermediate of NAD+ Synthesis, Protects the Heart from Ischemia and Reperfusion
|PLoS ONE|2014|295
Activation of Mst1 causes dilated cardiomyopathy by stimulating apoptosis without compensatory ventricular myocyte hypertrophy
|Journal of Clinical Investigation|2003|277
A functional interaction between Hippo-YAP signalling and FoxO1 mediates the oxidative stress response
|Nature Communications|2014|274
Inhibition of endogenous thioredoxin in the heart increases oxidative stress and cardiac hypertrophy
|Journal of Clinical Investigation|2003|235
The MEKK1-JNK pathway plays a protective role in pressure overload but does not mediate cardiac hypertrophy
|Journal of Clinical Investigation|2002|168