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Kv4.3通道蛋白作为瞬时外向钾电流的核心功能结构,在心肌细胞早期复极化中发挥重要作用.Kv4.3通道蛋白下调致使动作电位时程延长,钙离子内流增加,从而影响心肌细胞钙调节和兴奋收缩耦联;增加的胞内钙离子激活钙/钙调素依赖性蛋白激酶Ⅱ(CaMKⅡ)和钙调神经磷酸酶,导致心肌肥厚和心力衰竭的发生.此外,Kv4.3通道蛋白下调促使CaMKⅡ从Kv4.3-CaMKⅡ复合物中分离并激活,加速心力衰竭过程.上调Kv4.3通道蛋白可抑制CaMKⅡ过度活化及其严重后果,可能是治疗心力衰竭的一大靶点.“,”Kv4.3 K +channel,the core of the transient outward potassium current (Ito) functional structure,plays a crucial role in the early phase of repolarization of myocardial cells .The downregulation of Kv4.3 K +channel leads to prolongation of action potential duration ( APD) and increase of intercellular Ca 2+,thus affecting Ca 2+handling and excitation-contraction coupling in the myocardial cells .Moreo-ver,increased intracellular Ca 2+could activate calcium/calmodulin dependent protein kinase Ⅱ( CaMKⅡ) and calmodulin neural phospha-tase,which is linked to the development of myocardial hypertrophy and heart failure .In addition,downregulated Kv4.3 K +channel leads to CaMKⅡdissociation from Kv4.3-CaMKⅡcomplex and then activates isolated CaMKⅡ,which accellerates heart failure process .Upregula-tion of Kv4.3 K +channel inhibits excessive activation of CaMKⅡand its related harmful consequences ,hence this is likely a potential target for the therapy of heart failure .