Non-ion channel therapeutics for heart failure and atrial fibrillation: Are CaMKII inhibitors ready for clinical use?

The Ca2+-calmodulin dependent protein kinase II (CaMKII) is an established central mediator of electro-physiological and contractile responses to cardiac stress, and its hyper-activation in cardiac diseases has been linked to heart failure (HF) and arrhythmia. Here we summarize the evidence supporting the role of CaMKII as a critical nodal point for therapeutic intervention against HF and atrial and ventricular tachyarrhythmias. Targeting of CaMKII in heart with inhibitors possessing appropriate selectivity might represent a novel therapeutic approach for HF and arrhythmias.

钙/钙调蛋白依赖性蛋白激酶II（CaMKII）是心脏应激的电生理和收缩反应的既定核心介质，其在心脏疾病中的过度激活与心力衰竭（HF）和心律失常有关。在此我们总结了支持CaMKII作为针对心力衰竭以及房性和室性快速性心律失常进行治疗干预的关键节点这一作用的证据。在心脏中使用具有适当选择性的抑制剂靶向CaMKII可能代表一种针对心力衰竭和心律失常的新型治疗方法。