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

Conclusions
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.

Source: Cardiovascular Research - January 22, 2017 Category: Cardiology Authors: Li, L., Li, J., Drum, B. M., Chen, Y., Yin, H., Guo, X., Luckey, S. W., Gilbert, M. L., McKnight, G. S., Scott, J. D., Santana, L. F., Liu, Q. Tags: Cardiac biology and remodelling Source Type: research