Left ventricular response in the transition from hypertrophy to failure recapitulates distinct roles of Akt, β-arrestin-2, and CaMKII in mice with aortic regurgitation

Aortic regurgitation (AR) is characterized by volume overload-induced eccentric hypertrophy due to diastolic reflux of blood from the aorta into the left ventricle (LV) (1,2). The Framingham Heart Study reported that the overall prevalence of AR was 13% in men and 8.5% in women (1,3). It’s anticipated that the prevalence of AR will increase even further due to the rapidly growing aged population worldwide (3,4). Although laudable progress has been made in the management of AR, the pathophysiological mechanisms involved in chronic AR remain not fully elucidated (5). Moreover, although mouse models of cardiac disease are common, in part because of abundant knowledge of their genome, appropriate and clinically relevant mouse models of AR for investigation of its impact on cardiac remodeling are still not fully ascertained (6)