Long-Term Biased β-Arrestin Signaling Improves Cardiac Structure and Function in Dilated Cardiomyopathy

Biased agonism of the angiotensin II receptor is known to promote cardiac contractility. Our laboratory indicated that these effects may be attributable to changes at the level of the myofilaments. However, these signaling mechanisms remain unknown. Because a common finding in dilated cardiomyopathy is a reduction in the myofilament-Ca 2 + response, we hypothesized that β-arrestin signaling would increase myofilament-Ca 2 + responsiveness in a model of familial dilated cardiomyopathy and improve cardiac function and morphology.