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

molecular biology more details view paper

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Excessive O-GlcNAcylation causes heart failure and sudden death

molecular biology more details view paper

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

molecular biology more details view paper

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PDE1 inhibition modulates Cav1.2 channel to stimulate cardiomyocyte contraction

pharmacology and toxicology more details view paper

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