Thioredoxin-1 maintains mechanistic target of rapamycin (mTOR) function during oxidative stress in cardiomyocytes
Shinichi Oka(National Center for Global Health and Medicine), Junichi Sadoshima(Rutgers, The State University of New Jersey)
Cited by 51
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