Key result
Abnormal RyR2 phosphorylation linked to heart failure, AF, and ventricular arrhythmias.
Advancing our understanding of RyR2 regulation is critical as it represents a unique and promising therapeutic target for heart failure and arrhythmias.
RyR2 phosphorylation should not yet guide therapy in HF or arrhythmias; extends CaMKII-S2814 consistency while leaving PKA-S2808 effects open.
Cardiac ryanodine receptor type 2 plays a key role in excitation-contraction coupling. The ryanodine receptor type 2 channel protein is modulated by various post-translational modifications, including phosphorylation by protein kinase A and Ca(2+)/calmodulin protein kinase II. Despite extensive research in this area, the functional effects of ryanodine receptor type 2 phosphorylation remain disputed. In particular, the potential involvement of increased ryanodine receptor type 2 phosphorylation in the pathogenesis of heart failure and arrhythmias remains a controversial area, which is discussed in this review article.
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Dobrev et al. (2014) conducted a review in Heart failure and arrhythmias. Ryanodine receptor type-2 (RyR2) phosphorylation was evaluated. Abnormal PKA- and CaMKII-dependent phosphorylation of RyR2 may contribute to the pathogenesis of heart failure, atrial fibrillation, and ventricular arrhythmias.
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