Loss of AKAP150 promotes pathological remodelling and heart failure propensity by disrupting calcium cycling and contractile reserve

Conclusions</div>These findings define a critical role for AKAP150 in regulating Ca²⁺cycling and myocardial ionotropy following pathological stress, suggesting the AKAP150 signalling pathway may serve as a novel therapeutic target for heart failure.</span>

Source: Cardiovascular Research - November 15, 2016 Category: Cardiology Source Type: research