Key result
Heart failure progression in a canine model was associated with destabilized RyR2 activity due to excessive CaMKII phosphorylation and oxidation, driving arrhythmogenesis and contractile dysfunction.
Authors
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Should not yet change HF practice; hypothesis-generating for CaMKII-RyR2 targeting in translational models.
Belevych et al. (2011) studied Heart failure. Heart failure progression in a canine model was associated with destabilized RyR2 activity due to excessive CaMKII phosphorylation and oxidation, driving arrhythmogenesis and contractile dysfunction.
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