Key result
CaMKII inhibition appears to protect against atrial fibrillation in animal models and correct proarrhythmic, defective intracellular Ca(2+) homeostasis in fibrillating human atrial cells.
Why the study?
Does CaMKII inhibition protect against atrial fibrillation and correct proarrhythmic intracellular Ca(2+) homeostasis?
Does CaMKII inhibition protect against atrial fibrillation and correct proarrhythmic intracellular Ca(2+) homeostasis?
This review highlights CaMKII as a nodal proarrhythmic signal in atrial fibrillation, suggesting CaMKII inhibition as a potential therapeutic strategy.
CaMKII inhibition merits clinical trials in AF; leaves open translation from animal and cellular data.
CaMKII is a serine-threonine protein kinase that is abundant in myocardium. Emergent evidence suggests that CaMKII may play an important role in promoting atrial fibrillation (AF) by targeting a diverse array of proteins involved in membrane excitability, cell survival, calcium homeostasis, matrix remodelling, inflammation, and metabolism. Furthermore, CaMKII inhibition appears to protect against AF in animal models and correct proarrhythmic, defective intracellular Ca(2+) homeostasis in fibrillating human atrial cells. This review considers current concepts and evidence from animal and human studies on the role of CaMKII in AF.
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Mesubi et al. (2016) conducted a review in Atrial fibrillation. CaMKII inhibition was evaluated. CaMKII inhibition appears to protect against atrial fibrillation in animal models and correct proarrhythmic, defective intracellular Ca(2+) homeostasis in fibrillating human atrial cells.
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