Key result
CaMKII overexpression drives heart failure by inducing RyR-mediated sarcoplasmic reticulum calcium leak.
Population
Myocardium of patients with heart failure and transgenic mouse models
Design
Review
Authors
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May support CaMKII inhibition trials in HF; leaves open translation from mouse models to patients.
CaMKII overexpression and subsequent RyR hyperphosphorylation represent a key mechanism in the pathogenesis of heart failure via sarcoplasmic reticulum calcium leak.
Lars S. Maier (2005) conducted a review in Heart failure and cardiac hypertrophy. CaMKIIdelta overexpression was evaluated. CaMKII overexpression leads to heart failure, with CaMKII-dependent RyR hyperphosphorylation acting as a novel mechanism causing sarcoplasmic reticulum calcium leak.
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