Functional Regulation of K Channels and Mutant Insight Into Clinical Therapeutic Strategies in Cardiovascular Diseases.

ATP-sensitive potassium channels (K channels) play pivotal roles in excitable cells and link cellular metabolism with membrane excitability. The action potential converts electricity into dynamics by ion channel-mediated ion exchange to generate systole, involved in every heartbeat. Activation of the K channel repolarizes the membrane potential and decreases early afterdepolarization (EAD)-mediated arrhythmias. K channels in cardiomyocytes have less function under physiological conditions but they open during severe and prolonged anoxia due to a reduced ATP/ADP ratio, lessening cellular excitability and thus preventing action potential generation and cell contraction. Small active molecules activate and enhance the opening of the K channel, which induces the repolarization of the membrane and decreases the occurrence of malignant arrhythmia. Accumulated evidence indicates that mutation of K channels deteriorates the regulatory roles in mutation-related diseases. However, patients with mutations in K channels still have no efficient treatment. Hence, in this study, we describe the role of K channels and subunits in angiocardiopathy, summarize the mutations of the K channels and the functional regulation of small active molecules in K channels, elucidate the potential mechanisms of mutant K channels and provide insight into clinical therapeutic strategies.