Figures & data
Figure 2. Tunicamycin-induced UPR activation alters the morphology of the action potential with prolonged action potential duration and decreased dV/dtmax of hiPSC-CMs, by decreasing all major cardiac ion channel currents.
![Figure 2. Tunicamycin-induced UPR activation alters the morphology of the action potential with prolonged action potential duration and decreased dV/dtmax of hiPSC-CMs, by decreasing all major cardiac ion channel currents.](/cms/asset/56996e70-129b-4a07-825a-fc1f6196ba01/kchl_a_1516985_f0002_oc.jpg)
Figure 3. A summarized scheme of the UPR regulation on human cardiac ion channels. Activated UPR downregulates selective ion channels, leads to prolonged APD and reduced dV/dtmax, which can contribute to electrical remodeling and arrhythmias. The PERK branch downregulates Nav1.5, Kv4.3, hERG, and KvLQT1, while the IRE1 branch downregulates Nav1.5, Cav1.2, hERG, and KvLQT1.
![Figure 3. A summarized scheme of the UPR regulation on human cardiac ion channels. Activated UPR downregulates selective ion channels, leads to prolonged APD and reduced dV/dtmax, which can contribute to electrical remodeling and arrhythmias. The PERK branch downregulates Nav1.5, Kv4.3, hERG, and KvLQT1, while the IRE1 branch downregulates Nav1.5, Cav1.2, hERG, and KvLQT1.](/cms/asset/305c3c3b-dcdc-4f46-b3f2-c204fdea6ad8/kchl_a_1516985_f0003_oc.jpg)