AAV9.I-1c Delivered Via Direct Coronary Infusion in a Porcine Model of Heart Failure Improves Contractility and Mitigates Adverse Remodelling

摘要

BackgroundHeart failure is characterised by impaired function and disturbed Ca²⁺ homeostasis. Transgenic increases in inhibitor-1 activity have been shown to improve Ca² cycling and preserve cardiac performance in the failing heart. The aim of this study is to evaluate the effect of activating the inhibitor (I-1c) of protein phosphatase 1 (I-1) through gene transfer on cardiac function in a porcine model of heart failure induced by myocardial infarction (MI).