Yasuhiro Nishino

Ischemic preconditioning activates AMPK in a PKC-dependent manner and induces GLUT4 up-regulation in the late phase of cardioprotection.

K. Shimamoto, T. Miura, T. Miki, 2004, Cardiovascular research.

Does enhanced expression of the Na+-CA2+ exchanger increase myocardial vulnerability to ischemia/reperfusion injury in rabbit hearts?

K. Shimamoto, T. Miura, T. Miki, 2003, Molecular and Cellular Biochemistry.

Blockade of Angiotensin II Type 1 Receptors Suppressed Free Radical Production and Preserved Coronary Endothelial Function in the Rabbit Heart After Myocardial Infarction

K. Shimamoto, T. Miura, A. Kuno, 2002, Journal of cardiovascular pharmacology.

Constitutive glycogen synthase kinase-3α/β activity protects against chronic β-adrenergic remodelling of the heart

René M. Botnar, Simon J. Walker, A. Shah, 2010, Cardiovascular research.

The Role of RIP2 in p38 MAPK Activation in the Stressed Heart*

R. Flavell, M. Cotten, Koichi S. Kobayashi, 2008, Journal of Biological Chemistry.

Glycogen Synthase Kinase-3 Inactivation Is Not Required for Ischemic Preconditioning or Postconditioning in the Mouse

A. Shah, D. Yellon, S. Davidson, 2008, Circulation research.

The role of RIP2 in p38 MAPK activation in the stressed heart

R. Flavell, M. Cotten, Koichi S. Kobayashi, 2008 .

Intracardiac fibroblasts, but not bone marrow derived cells, are the origin of myofibroblasts in myocardial infarct repair.

K. Shimamoto, T. Miura, T. Miki, 2005, Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology.

Granulocyte colony stimulating factor/macrophage colony stimulating factor improves postinfarct ventricular function by suppression of border zone remodelling in rats ‡

K. Shimamoto, T. Miura, N. Ura, 2004, Clinical and experimental pharmacology & physiology.

Mitochondrial ATP-sensitive K+ channels play a role in cardioprotection by Na+-H+ exchange inhibition against ischemia/reperfusion injury.

Yongge Liu, K. Shimamoto, A. Nakano, 2001, Journal of the American College of Cardiology.

Contribution of both the sarcolemmal KATP and mitochondrial KATP channels to infarct size limitation by KATP channel openers: differences from preconditioning in the role of sarcolemmal KATP channels

K. Shimamoto, T. Miura, T. Miki, 2001, Naunyn-Schmiedeberg's Archives of Pharmacology.