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Impaired sarcoplasmic reticular (SR) Ca2+ uptake resulting from decreased SR Ca2+-ATPase type 2a (SERCA2a) expression or activity is characteristic of heart failure (HF) with its associated ventricular arrhythmias. Recent attempts at gene therapy of these conditions explored strategies enhancing SERCA2a expression and/or activity as novel approaches to HF management. We here explore the role of Pak1 in maintaining ventricular Ca2+ homeostasis and electrophysiological stability under both physiological and.acute β-adrenergic or hypertrophic challenge conditions

Original publication




Journal article


Cardiovasc Res

Publication Date



103 Suppl 1