Elizabeth D. Luczak

This study shows chronic CaMKII activation drives skeletal muscle aging and sarcopenia, and partial inhibition in aged muscle improves function and shifts the transcriptome toward a youthful state.

The paper uses a CaMKII activity reporter to study activation patterns in cardiac, skeletal muscle, and neurons, revealing differences in activation rates and subcellular localization.

This study shows SGLT2 inhibitors reduce diabetic cardiomyopathy and atrial fibrillation risk in T2D mice, but their effects are not dependent on CaMKII inhibition.

The paper develops a CaMKII biosensor for high-throughput screening and identifies ruxolitinib as a potent and cardioprotective CaMKII inhibitor effective in preventing atrial fibrillation.

This paper shows that excessive O-GlcNAcylation causes heart failure and sudden death in mice, while reducing it protects against cardiac stress.

This study shows mitochondrial CaMKII activation leads to metabolic reprogramming, energetic insufficiency, and dilated cardiomyopathy, with potential therapeutic targets identified.

This study shows that O-GlcNAcylation and oxidative stress via CaMKII contribute to atrial fibrillation in type 1 and type 2 diabetes through distinct mechanisms.