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

ABSTRACT:

Background

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-Ca²⁺ response, we hypothesized that β-arrestin signaling would increase myofilament-Ca²⁺ responsiveness in a model of familial dilated cardiomyopathy and improve cardiac function and morphology.

Methods

We treated a dilated cardiomyopathy-linked mouse model expressing a mutant tropomyosin (Tm-E54K) for 3 months with either TRV120067, a β-arrestin 2-biased ligand of the angiotensin II receptor

SUBMITTER: Ryba DM 

PROVIDER: S-EPMC5350031 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature