The Role of Casein Kinase 2 in Ion Channel Remodeling After Myocardial Infarction: Editorial to: “Valsartan Upregulates Kir2.1 in Rats Suffering from Myocardial Infarction via Casein Kinase 2” by Xinran Li et al.

摘要

Cardiac remodeling is a necessary process in the context of physiological adaptation during normal growth according to the demand of alterations, including changes in contractility and beating rate. However, malfunctional remodeling due to pathological conditions is an ultimate disaster in disease pathogenesis, which leads to a poor outcome and high mortality [1]. Besides the cardiac enlargement of ventricular volume after myocardial infarction (MI), dysfunction due to electrophysiological remodeling such as a decrease in delayed rectifier potassium currents (IK) is a prominent feature showing reduced survival in patients with heart disease [2]. Cardiac inward rectifying potassium currents (Ik1) play an important role in shaping action potentials, which is a key character representing the electrical activity made by a multitude of various ion channels and transporters [3]. The cardiac IK1 stabilizes the resting membrane potential and is responsible for shaping the initial depolarization and final repolarization of the action potential [4, 5]. Indeed, infarction generally entails significant cellular and molecular remodeling in the left ventricle, resulting in functional and biochemical alterations of the myocardium due to the modulation of IK1 [2].