Blockade of β-adrenoceptors restores the GRK2-mediated adrenal α2-adrenoceptor-catecholamine production axis in heart failure

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Adrenal Beta-Arrestin 1 Inhibition In Vivo Attenuates Post-Myocardial Infarction Progression to Heart Failure and Adverse Remodeling Via Reduction of Circulating Aldosterone Levels

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Adrenal GRK2 lowering is an underlying mechanism for the beneficial sympathetic effects of exercise training in heart failure

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Comparative Cardiac Gene Delivery of Adeno-Associated Virus Serotypes 1-9 reveals that AAV6 Mediates the Most Efficient Transduction in Mouse Heart

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Reduction of Sympathetic Activity via Adrenal-targeted GRK2 Gene Deletion Attenuates Heart Failure Progression and Improves Cardiac Function after Myocardial Infarction

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GRK2 as a novel gene therapy target in heart failure

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An adrenal  -arrestin 1-mediated signaling pathway underlies angiotensin II-induced aldosterone production in vitro and in vivo

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Myocardial Adeno-Associated Virus Serotype 6–βARKct Gene Therapy Improves Cardiac Function and Normalizes the Neurohormonal Axis in Chronic Heart Failure

(2008) Giuseppe Rengo et al.   CIRCULATION

G Protein–Coupled Receptor Kinase 2 Ablation in Cardiac Myocytes Before or After Myocardial Infarction Prevents Heart Failure

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Modulation of Adrenal Catecholamine Secretion by In Vivo Gene Transfer and Manipulation of G Protein–coupled Receptor Kinase-2 Activity

(2008) Anastasios Lymperopoulos et al.   MOLECULAR THERAPY