Calcium/Calmodulin-Dependent Protein Kinase II Activity Persists During Chronic {beta}-Adrenoceptor Blockade in Experimental and Human Heart Failure [Original Articles]

Conclusions—
Chronic β-AR blocker therapy in patients and in a mouse model of CaMKII-induced HF is not associated with a change in CaMKII activity. Thus, our data suggest that the molecular effects of β-AR blockers are not based on a modulation of CaMKII. Directly targeting CaMKII may, therefore, further improve HF therapy in addition to β-AR blockade.

Source: Circulation: Heart Failure - May 9, 2017 Category: Cardiology Authors: Dewenter, M., Neef, S., Vettel, C., Lammle, S., Beushausen, C., Zelarayan, L. C., Katz, S., von der Lieth, A., Meyer-Roxlau, S., Weber, S., Wieland, T., Sossalla, S., Backs, J., Brown, J. H., Maier, L. S., El-Armouche, A. Tags: Animal Models of Human Disease, Mechanisms, Heart Failure, Pharmacology Original Articles Source Type: research