William Kutschke

TL;DR: It is shown that oxidation of paired regulatory domain methionine residues sustains CaMKII activity in the absence of Ca2+/CaM and highlights the critical importance of oxidation-dependent CaMK II activation to AngII and ischemic myocardial apoptosis.

TL;DR: A role for GSK-3β is revealed as an inhibitor of hypertrophic signaling in the intact myocardium and it is suggested that elevation of cardiac GSK -3β activity may provide clinical benefit in the treatment of pathologic hypertrophy and heart failure.

TL;DR: In this experimental setting, calcineurin blockade with CsA prevented LV hypertrophy due to pressure overload in mice and in vivo parameters of ventricular volume and function were examined using echocardiography.

TL;DR: The findings suggest that activation of a mitochondrial/ox-CaMKII pathway contributes to increased sudden death in diabetic patients after myocardial infarction.

TL;DR: A computational model of the sinoatrial node showed that a loss of SAN cells below a critical threshold caused SND by preventing normal impulse formation and propagation, and suggested that targeted CaMKII inhibition may be useful for preventing SND in high-risk patients.