PRJNA837990
studies of iPS-CMs overexpressing KCNJ2
iPSC-derived cardiomyocytes (iPSC-CMs) are relatively electrophysiologically and structurally immature compared to primary cardiomyocytes, hindering their widespread application in basic and translational research. The inwardly rectifying potassium channel Kir2.1, encoded by KCNJ2, plays a major role in the plateau phase of cardiac action potential repolarization, helping to stabilize the resting membrane potential. However, due to the lower current density of IK1 encoding Kir2.1, iPSC-CMs are prone to exhibit auto-arrhythmias and further exhibit slower sodium uptake as well as impaired sarcoplasmic reticulum-mediated calcium handling. In this project, normal human iPSC-CMs were obtained by myocardial directional differentiation technology, and a lentivirus-mediated KCNJ2 overexpression system of iPSC-CMs was constructed. The effect and mechanism of expression on the maturation of iPSC-CMs will open up new avenues for promoting the maturation of iPSC-CMs and subsequent applications.