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. 2022 Dec 30;132(2):187–204. doi: 10.1161/CIRCRESAHA.122.321398

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© 2023 The Authors.

Circulation Research is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 3. — NOTCH1 disruption alters electrophysiological behaviors of human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) by shortening action potential durations. A, Representative ventricular-, atrial-, and nodal-like electrophysiological characteristics in iPSC-CMs inferred by optical mapping. B, Percentages of ventricular-, atrial-, and nodal-like cardiomyocytes in wild-type (WT) and NOTCH1 knockout (N1KO) iPSC-CMs. C and D, APD90, APD50, and APD90/APD50 in wild-type (WT; n=20) and N1KO (n=20) iPSC-CMs measured by whole-cell patch clamp (t test, n=20). E, Patch clamp analysis shows shortened repolarization phase in N1KO versus WT iPSC-CMs. F and G, Transient outward K+ current is increased in N1KO (F) compared with WT (G) iPSC-CMs. H – J, Delayed rectifier K+ current (I_Kr tail current) is increased in N1KO (H) versus WT (I) iPSC-CMs. K – M, Inward Na+ currents are reduced in N1KO (K) compared with WT (L) iPSC-CMs across different member potentials. N and O, Amplitudes of inward Ca²⁺ currents are decreased in N1KO (N) versus WT (O) iPSC-CMs. Data are presented as mean±SEM. *P<0.05, **P<0.01.