Jonathan M. Granger

Myocardial STIM1 deficiency triggers mitochondrial fission to impair electrophysiological function and exacerbate post-MI remodeling

This study shows that reducing STIM1 in cardiomyocytes causes mitochondrial fragmentation and metabolic changes, leading to electrical instability and worsened heart function after a heart attack.

Endothelial Rho kinase controls blood vessel integrity and angiogenesis

This study investigates the role of endothelial Rho kinase (ROCK1/2) in vascular integrity and angiogenesis, finding that their loss leads to vascular defects and lethality.

Transient AMPK activation by nutrient stress of high fat diet preserves cardiac electrophysiological stability and protects against arrhythmias

This study shows that AMPK activation by high-fat diet reduces arrhythmia risk by improving cardiac electrophysiology and mitochondrial function.

Novel Biosensor Identifies Ruxolitinib as a Potent and Cardioprotective CaMKII Inhibitor

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.

Excessive O-GlcNAcylation causes heart failure and sudden death

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

Mitochondrial CaMKII causes metabolic reprogramming, energetic insufficiency, and dilated cardiomyopathy

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

O-GlcNAcylation, oxidation and CaMKII contribute to atrial fibrillation in type 1 and type 2 diabetes by distinct mechanisms

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.